2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T41e,Highlights across studies: - **Atopic march ML model:** Simplified models using routine early-life clinical features accurately predicted moderate-to-severe persistent asthma/allergic rhinitis by ages 5–11. - **Peanut OIT (IMPACT follow-up):** 80% of children who received pnOIT only (group A, n=40) were eating peanut at follow-up; 35% of group A reported peanut reactions since IMPACT; IgG4:IgE ratio remained higher in the pnOIT group vs. placebo years later. - **Dupilumab & autoimmunity in children:** Cutaneous autoimmune diagnoses (mainly psoriasis and alopecia areata) were ~2 per 1,000 children/year higher in the dupilumab group; no significant differences in endocrine, GI, or rheumatologic autoimmune diagnoses. - **EoE transcriptome:** Dupilumab normalized >1,300 dysregulated EoE genes (eosinophil and non-eosinophil pathways) across all age groups, sustained on treatment. - **α-Gal IgG & atherosclerosis:** Anti-α-Gal IgG formed immune complexes with α-Gal–bearing LDL, enhancing macrophage uptake and foam cell formation in vitro.31:T433,Increasing evidence from preclinical models has linked the actions of brown adipose tissue (BAT) with protection against atherosclerosis and cardiovascular disease, in part due to its salutary effects on systemic lipid composition. However, human data on the role of BAT in atherosclerosis are scarce. In this cross-sectional study, we examined 65 individuals with obesity and analyzed cold-induced BAT activity and vascular inflammation in the aorta using We identified 21 subjects with cold-induced BAT (BAT positive), whereas 44 individuals had no significant BAT activity (BAT negative) after cold exposure. Both groups had similar age, sex distribution, body mass index, and classical cardiovascular risk profile. However, BAT-positive individuals had significantly less arterial inflammation as evidenced by lower Together, these data link human BAT function with protection against arterial inflammation and a potentially antiatherogenic and anti-inflammatory circulating profile. URL: https://www.clinicaltrials.gov; Unique identifiers: NCT02381483 and NCT03168009.32:Td0e, BACKGROUND: Increasing evidence from preclinical models has linked the actions of brown adipose tissue (BAT) with protection against atherosclerosis and cardiovascular disease, in part due to its salutary effects on systemic lipid composition. However, human data on the role of BAT in atherosclerosis are scarce. METHODS: In this cross-sectional study, we examined 65 individuals with obesity and analyzed cold-induced BAT activity and vascular inflammation in the aorta using 18 F-fluorodeoxyglucose positron emission tomography combined with computed tomography in combination with systemic lipidomics and proteomics analyses. RESULTS: We identified 21 subjects with cold-induced BAT (BAT positive), whereas 44 individuals had no significant BAT activity (BAT negative) after cold exposure. Both groups had similar age, sex distribution, body mass index, and classical cardiovascular risk profile. However, BAT-positive individuals had significantly less arterial inflammation as evidenced by lower 18 F-fluorodeoxyglucose uptake in the ascending aorta and the aortic arch. Notably, BAT volume, SUV mean , and cold-induced thermogenesis correlated negatively with aortic inflammation, suggesting an atheroprotective role of BAT. Using unbiased lipidomics and proteomics analyses in plasma, we found that anti-inflammatory and potentially antiatherogenic circulating factors, such as cytochrome P450 oxylipin products and the serpin family member SERPINB12, were increased in BAT positive, whereas proatherogenic and prothrombotic factors, including acute phase protein ORM2 (orosomucoid 2), APOD (apolipoprotein D), FGA (fibrinogen A), and FGB (fibrinogen B), were significantly lower in individuals with active BAT. Likewise, the circulating concentrations of inflammatory markers, such as IL-6 (interleukin-6), were reduced in BAT positive versus BAT negative. CONCLUSIONS: Together, these data link human BAT function with protection against arterial inflammation and a potentially antiatherogenic and anti-inflammatory circulating profile. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifiers: NCT02381483 and NCT03168009 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Atherosclerosis: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Atherosclerosis (condition). Clinician-written summaries and actionable practice insights. Updated daily.\",\"url\":\"https://www.reachrx.ai/hub/tag/condition/Atherosclerosis\",\"breadcrumb\":{\"@type\":\"BreadcrumbList\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Home\",\"item\":\"https://www.reachrx.ai\"},{\"@type\":\"ListItem\",\"position\":2,\"name\":\"Research Hub\",\"item\":\"https://www.reachrx.ai/hub\"},{\"@type\":\"ListItem\",\"position\":3,\"name\":\"Conditions\",\"item\":\"https://www.reachrx.ai/hub/tag/condition\"},{\"@type\":\"ListItem\",\"position\":4,\"name\":\"Atherosclerosis\",\"item\":\"https://www.reachrx.ai/hub/tag/condition/Atherosclerosis\"}]}}"}}]],["$","$L2f",null,{"title":"Atherosclerosis: Research & Clinical Takeaways","description":"Discover peer-reviewed research on Atherosclerosis with concise clinician summaries and next-step guidance.","papers":[{"doi":"10.1161/jaha.125.048286","pmid":"42714574","title":"Haptoglobin and Immunoglobulin A2 Predict Cardiovascular Risk in Asymptomatic Subjects: The BioImage Study","journal_title":"Journal of the American Heart Association","journal_issn":"2047-9980","published_at":"2026-09-09T00:00:00.000Z","url":"https://doi.org/10.1161/jaha.125.048286","source_score":33,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-12T06:20:14.469Z","updated_at":"2026-09-12T06:20:14.469Z","tags":[{"paper_doi":"10.1161/jaha.125.048286","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"condition","value":"Subclinical Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"generic","value":"haptoglobin","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"generic","value":"high-sensitivity C-reactive protein","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"generic","value":"immunoglobulin A2","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"modality","value":"Biomarker","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"sample_size","value":"n=5328","value_numeric":5328},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"study_design","value":"Prospective Cohort Study","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"warning","value":"Haptoglobin and IgA2 are not yet standard clinical assays; immunoturbidimetry was used here, but assay availability and standardization may vary across health systems.","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"warning","value":"The incremental improvement in risk prediction with combined biomarker assessment was described as 'modest' but the absolute NRI/IDI or C-statistic changes are not reported in the abstract — clinicians should review full results for precise reclassification metrics.","value_numeric":null},{"paper_doi":"10.1161/jaha.125.048286","tag_type":"warning","value":"The study validated findings from European cohorts in a US population, but the at-risk, older sample (mean age 69) may limit applicability to general primary prevention populations or younger age groups.","value_numeric":null}],"summaries":{"what_studied":"This study evaluated whether plasma haptoglobin and IgA2 predict major cardiovascular adverse events (MACE) and all-cause mortality in 5,328 asymptomatic US adults (mean age 69, 56.9% women) from the BioImage study, beyond traditional Framingham Risk Score (FRS) and vascular imaging (carotid plaque burden, coronary artery calcium) over a median follow-up of 4.6 years.","key_result":"466 participants (8.8%) experienced the composite endpoint. Haptoglobin and IgA2 independently predicted MACE and all-cause death beyond FRS and imaging. Individuals with high levels of both biomarkers (above median) had a ~2-fold higher event rate than those with low levels. Combined biomarker assessment modestly but significantly improved risk prediction over FRS and imaging alone.","limitations":"- Median follow-up of only 4.6 years may miss longer-term risk trajectories.\n- Study population was older (mean age 69) and at-risk, limiting generalizability to younger or lower-risk primary prevention populations.\n- Biomarker improvement in risk prediction was described as modest, leaving the clinical magnitude of incremental benefit uncertain.","practice_takeaway":"In asymptomatic older adults, measuring plasma haptoglobin and IgA2 may add meaningful risk information on top of standard risk scores and imaging — consider them as adjunct biomarkers for cardiovascular risk stratification in primary prevention settings. Patients with both biomarkers above the median carry roughly twice the event rate and may warrant closer follow-up or more aggressive risk-factor management."}},{"doi":"10.1038/s41581-026-01117-6","pmid":"42697978","title":"Inflammation as a therapeutic target to improve kidney and cardiovascular outcomes","journal_title":"Nature Reviews Nephrology","journal_issn":"1759-5061","published_at":"2026-09-04T00:00:00.000Z","url":"https://doi.org/10.1038/s41581-026-01117-6","source_score":9,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-08T06:32:03.090Z","updated_at":"2026-09-08T06:32:03.090Z","tags":[{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"brand","value":"Baricitinib","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"generic","value":"bardoxolone","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"generic","value":"baricitinib","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"generic","value":"pentoxifylline","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"generic","value":"ruboxistaurin","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"generic","value":"selonsertib","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"ASK1 Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"GLP-1 Receptor Agonist","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"IL-1β Monoclonal Antibody","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"IL-6 Monoclonal Antibody","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"Non-Steroidal Mineralocorticoid Antagonist","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"Nrf2 Activator","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"Phosphodiesterase Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"PKCβ Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"RAAS Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"warning","value":"Brand tag for baricitinib (Olumiant) was not explicitly named in the abstract; the generic name was used instead.","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"warning","value":"Level of evidence set to 7 (narrative expert review); no systematic search methodology or GRADE assessment is described in the abstract.","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01117-6","tag_type":"warning","value":"Several investigational agents discussed (selonsertib, ruboxistaurin) have had failed or halted clinical programs; the review may not fully reflect the most current trial statuses as of publication.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates inflammation as a therapeutic target in chronic kidney disease (CKD), examining how systemic and local inflammatory pathways drive kidney damage, atherosclerosis, and cardiac dysfunction, and assessing both investigational and proven anti-inflammatory treatments.","key_result":"Multiple inflammatory pathways (ASK1, JAK1/2, PKCβ, Nrf2, PDE, IL-1β, IL-6) have been targeted in CKD trials with mixed results; established therapies (RAAS inhibitors, SGLT2i, GLP-1 RAs, ns-MRAs) also carry anti-inflammatory properties that may partly explain their cardio-renal benefits.","limitations":"As a narrative review, it does not provide pooled effect sizes or head-to-head comparisons; several investigational agents (e.g., selonsertib, ruboxistaurin) have had limited or failed trial programs, and causality between inflammation reduction and hard outcomes remains incompletely established.","practice_takeaway":"Clinicians should recognize that hsCRP elevation signals heightened cardiovascular and CKD progression risk, and that selecting proven therapies with anti-inflammatory properties (SGLT2 inhibitors, GLP-1 receptor agonists, ns-MRAs, RAAS inhibitors) may provide additive benefit beyond blood pressure or glucose control alone."}},{"doi":"10.1038/s41569-026-01342-3","pmid":"42687017","title":"Intracoronary imaging in percutaneous coronary intervention: why, when, how and which from large, randomized trials","journal_title":"Nature Reviews Cardiology","journal_issn":"1759-5002","published_at":"2026-09-02T00:00:00.000Z","url":"https://doi.org/10.1038/s41569-026-01342-3","source_score":28,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-09T06:21:08.719Z","updated_at":"2026-09-09T06:21:08.719Z","tags":[{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"condition","value":"Coronary Artery Disease","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"modality","value":"Intracoronary Imaging","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"modality","value":"Intravascular Ultrasound","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"modality","value":"Optical Coherence Tomography","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"modality","value":"Percutaneous Coronary Intervention","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"study_design","value":"Systematic Review / Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"warning","value":"Full page content was not extracted from the PDF — only the abstract and metadata were available. Summary details are based solely on the abstract; specific event rates, hazard ratios, and per-trial results could not be verified from the full text.","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"warning","value":"Study design tagged as 'Systematic Review / Narrative Review' based on abstract framing; the paper is described as a 'Review' synthesizing RCT evidence rather than a formal meta-analysis.","value_numeric":null},{"paper_doi":"10.1038/s41569-026-01342-3","tag_type":"warning","value":"The 'practice_changing' impact flag reflects the synthesis of eight large RCTs and the authors' stated aim of reshaping clinical decision-making for ICI use in PCI; individual trial results were mixed.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates the clinical use of intracoronary imaging (ICI) — specifically IVUS and OCT — to guide percutaneous coronary intervention (PCI) in patients with coronary artery disease, synthesizing findings from eight large (n > 1,000) international randomized trials: ILUMIEN IV, IVUS-ACS, IVUS-CHIP, IVUS-XPL, OCCUPI, OCTOBER, RENOVATE-COMPLEX-PCI, and ULTIMATE.","key_result":"Across eight large randomized trials, ICI-guided PCI generally improved clinical outcomes compared with angiography-guided PCI, though results were heterogeneous; benefits were most consistent in complex lesion subsets and high-risk populations, while routine use in all-comers showed mixed findings.","limitations":"- Full text page content was not extractable, limiting granular data verification (e.g., absolute event rates per trial).\n- Heterogeneity in study populations and lack of standardized ICI optimization criteria across trials complicates cross-trial comparisons.\n- Mixed trial results leave uncertainty about which specific patient or lesion subgroups benefit most from ICI guidance in real-world practice.","practice_takeaway":"Clinicians should prioritize ICI guidance — IVUS or OCT — for complex PCI cases (e.g., ACS, calcified or long lesions), where the evidence for outcome benefit is most consistent. Patient selection and standardized ICI protocols are key to translating trial benefits to everyday practice."}},{"doi":"10.1056/nejmoa2609059","pmid":"42670946","title":"Prevalence of Silent Atherosclerosis across Adult Life","journal_title":"New England Journal of Medicine","journal_issn":"0028-4793","published_at":"2026-08-29T00:00:00.000Z","url":"https://doi.org/10.1056/nejmoa2609059","source_score":296,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-02T06:22:31.040Z","updated_at":"2026-09-02T06:22:31.040Z","tags":[{"paper_doi":"10.1056/nejmoa2609059","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"category","value":"Medicine, General & Internal","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"modality","value":"Coronary Computed Tomographic Angiography","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"modality","value":"Vascular Ultrasonography","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"sample_size","value":"n=16808","value_numeric":16808},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"study_design","value":"Prospective Cohort Study","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"warning","value":"Generalizability may be limited: participants were enrolled exclusively in Denmark and Spain, and racial/ethnic diversity of the cohort is not described in the abstract.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"warning","value":"The 'practice_changing' impact flag reflects the large sample size and striking prevalence findings, but should be interpreted cautiously until event-outcome data are available.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2609059","tag_type":"warning","value":"This paper was published August 29, 2026 — very recently. Longitudinal outcome data from the REACT cohort have not yet been reported; prevalence findings are cross-sectional only.","value_numeric":null}],"summaries":{"what_studied":"A prospective cohort study (REACT) in Denmark and Spain enrolled 16,808 adults aged 18–70 without known atherosclerotic cardiovascular disease across five age strata (balanced by sex) to define the age- and sex-specific prevalence, vascular territory distribution, and plaque volume of silent atherosclerosis using 3D vascular ultrasound of carotid/femoral arteries and coronary CT angiography.","key_result":"Silent atherosclerosis was present in 57.1% of participants overall (95% CI 56.3–58.0). Even in the youngest stratum (18–29 years), prevalence was 8.7% in men and 6.7% in women. Prevalence rose with age, with women showing a later but steeper midlife increase. Plaque volume grew exponentially with age and multiarterial involvement became more common; isolated coronary atherosclerosis was rare (≤9.3% men, ≤5.0% women in any stratum).","limitations":"Baseline-only data are reported here — longitudinal outcomes (events, mortality) are not yet available, so causal or prognostic inferences remain limited. Study was conducted in two European countries (Denmark and Spain), which may limit generalizability to other ethnicities and healthcare settings.","practice_takeaway":"Silent atherosclerosis is far more common than traditional risk-factor models suggest, affecting nearly 1 in 11 adults in their 20s and more than half of all adults by midlife. Clinicians should consider earlier, broader vascular screening strategies — particularly peripheral artery imaging — rather than focusing solely on coronary risk."}},{"doi":"10.1161/atvbaha.126.325070","pmid":"42657466","title":"Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis","journal_title":"Arteriosclerosis, Thrombosis, and Vascular Biology","journal_issn":"1079-5642","published_at":"2026-08-27T00:00:00.000Z","url":"https://doi.org/10.1101/2025.08.18.670994","source_score":17,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-04T06:22:21.511Z","updated_at":"2026-09-04T06:22:21.511Z","tags":[{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"condition","value":"Metabolic Syndrome","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"generic","value":"NaKtide","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"modality","value":"Na/K-ATPase Signaling Inhibitor","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"sample_size","value":"n=60","value_numeric":60},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"study_design","value":"Preclinical Animal Study","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"warning","value":"Sample sizes are small (n=3–10 per group) and vary across assays, limiting statistical power for some endpoints.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"warning","value":"The study used only male Apoe−/− mice; sex-specific and species-to-human generalizability is uncertain.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"warning","value":"This is a preprint posted on bioRxiv (August 2025); the journal listing as Arteriosclerosis, Thrombosis, and Vascular Biology with a 2026 publication date may indicate forthcoming or in-press status — peer-review completion could not be confirmed from the document.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.325070","tag_type":"warning","value":"Total N is estimated from reported per-group ranges across multiple experiments; an exact aggregate N is not stated.","value_numeric":null}],"summaries":{"what_studied":"This study tested whether blocking Na/K-ATPase (NKA) signaling specifically in adipocytes reduces atherosclerosis. Adipocyte-specific NaKtide (Adipo-NaKtide) was delivered via lentiviral vector under the adiponectin promoter in male *Apoe*−/− mice fed a Western diet for 12 weeks.","key_result":"Adipo-NaKtide cut atherosclerotic plaque area by **67%** in the aortic arch and **48%** in the aortic sinus. Macrophage (CD68+) and smooth muscle cell (α-SMA+) content in the aortic sinus fell by **45%** and **53%**, respectively. Plasma IL-6 dropped from ~297 to ~129 pg/ml, and TNF-α from ~9.1 to ~7.4 pg/ml. Glucose tolerance and adipose oxidative stress markers also improved.","limitations":"- The specific adipocyte-derived mediators driving vascular effects were not identified.\n- Study used only male mice in a single murine atherosclerosis model; human relevance is unestablished.\n- Long-term safety and off-target effects of systemic NKA inhibition remain unknown.","practice_takeaway":"Adipocyte NKA signaling is a meaningful upstream driver of atherosclerosis in this preclinical model, suggesting it could be a novel therapeutic target for cardiometabolic disease. Clinical translation requires human studies before any practice change."}},{"doi":"10.1038/s41585-026-01183-2","pmid":"42649386","title":"Erectile dysfunction and cardiovascular health","journal_title":"Nature Reviews Urology","journal_issn":"1759-4812","published_at":"2026-08-26T00:00:00.000Z","url":"https://doi.org/10.1038/s41585-026-01183-2","source_score":11,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-06T06:23:02.128Z","updated_at":"2026-09-06T06:23:02.128Z","tags":[{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"condition","value":"Endothelial Dysfunction","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"condition","value":"Erectile Dysfunction","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"modality","value":"Cardiovascular Risk Stratification","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"warning","value":"The abstract does not specify the number or types of studies reviewed, limiting assessment of evidence breadth.","value_numeric":null},{"paper_doi":"10.1038/s41585-026-01183-2","tag_type":"warning","value":"This is a review article published in 2026; no sample size is applicable and no original trial data are presented. The 'practice_changing' impact flag reflects the clinical reframing of ED as a cardiovascular sentinel marker, which may already be partially established in some guidelines.","value_numeric":null}],"summaries":{"what_studied":"This review examines the epidemiological and mechanistic links between erectile dysfunction (ED) and cardiovascular disease (CVD), including the roles of low-grade inflammation, endothelial dysfunction, and atherosclerosis, as well as diagnostic and management strategies.","key_result":"ED is identified as a sentinel and early marker of subclinical vascular disease; coronary artery calcium scoring and echocardiography are highlighted as useful tools for cardiovascular risk stratification in men with ED.","limitations":"As a review, no original patient-level data or effect sizes are reported; conclusions depend on the quality and heterogeneity of the underlying cited studies.","practice_takeaway":"Men presenting with ED should prompt clinicians to assess cardiovascular risk, potentially using coronary artery calcium scoring or echocardiography. Integrating sexual and cardiometabolic health management in this population may improve outcomes."}},{"doi":"10.1002/ctm2.70774","pmid":"42591007","title":"Space radiation impairs long‐term endothelial integrity and may promote atherosclerosis in ApoE‐deficient mice","journal_title":"Clinical and Translational Medicine","journal_issn":"2001-1326","published_at":"2026-08-13T00:00:00.000Z","url":"https://doi.org/10.1002/ctm2.70774","source_score":34,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-20T06:47:53.116Z","updated_at":"2026-08-20T06:47:53.116Z","tags":[{"paper_doi":"10.1002/ctm2.70774","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"condition","value":"Endothelial Dysfunction","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"condition","value":"Radiation-Induced Cardiovascular Injury","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"level_of_evidence","value":"6","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"modality","value":"Gamma Irradiation","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"modality","value":"Ionizing Radiation (Simulated Galactic Cosmic Ray)","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"study_design","value":"Animal Experimental Study","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"warning","value":"Gamma (400 cGy) and SimGCRSim (50 cGy) doses differ by 8-fold, making cross-group biological comparisons difficult to interpret; the authors acknowledge this limitation implicitly.","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"warning","value":"Sample size (total N) is not reported in the available text; the sample_size tag has been omitted accordingly.","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"warning","value":"Sex of mice is not explicitly stated in the full text; male sex is inferred from a cited companion study (Brojakowska et al. 2023) using male ApoE null mice — verify in supplementary methods.","value_numeric":null},{"paper_doi":"10.1002/ctm2.70774","tag_type":"warning","value":"This is a Letter to the Journal (pilot study), not a full research article; formal statistical power calculations and detailed methods are in supplementary materials not provided here.","value_numeric":null}],"summaries":{"what_studied":"This pilot study examined the long-term effects of simulated space radiation (NASA's SimGCRSim mixed galactic cosmic ray field at 50 cGy and gamma radiation at 400 cGy) on endothelial integrity and atherosclerotic plaque development in ApoE-deficient mice sacrificed at 16 months of age — more than one year post-irradiation.","key_result":"Both radiation types significantly reduced luminal CD31+ and VE-cadherin+ endothelial coverage and eNOS expression in aortic root plaques compared with sham controls. Gamma irradiation significantly increased atherosclerotic plaque area; SimGCRSim showed a similar trend reaching only borderline significance. No significant differences were found in plaque lipid content, fibrotic area, necrotic core, or inflammatory cell infiltration (CD45+/CD68+), though a non-significant ~2-fold increase in plaque calcification was seen in the SimGCRSim group.","limitations":"- Pilot study with small groups; SimGCRSim plaque area increase reached only borderline significance, limiting conclusions about atherosclerosis promotion.\n- Gamma (400 cGy) and SimGCRSim (50 cGy) doses differ substantially, making direct comparison of radiation-type effects difficult.\n- ApoE-null mice on normal chow are a surrogate model; mechanistic pathways were not explored.","practice_takeaway":"Deep-space radiation may cause lasting vascular endothelial damage and accelerate atherosclerosis well beyond one year after exposure, supporting the need for cardiovascular monitoring and countermeasure development for astronauts on long-duration missions. These findings are currently preclinical and require human validation before clinical translation."}},{"doi":"10.1016/j.jaci.2026.06.010","pmid":null,"title":"The Editors’ Choice","journal_title":"Journal of Allergy and Clinical Immunology","journal_issn":"0091-6749","published_at":"2026-08-05T00:00:00.000Z","url":"https://doi.org/10.1016/j.jaci.2026.06.010","source_score":3,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":false,"crossref":true,"unpaywall":true},"created_at":"2026-08-11T13:26:12.518Z","updated_at":"2026-08-24T06:18:18.582Z","tags":[{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"age_group","value":"pediatric","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"brand","value":"Dupixent","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"category","value":"Allergy","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Allergic Rhinitis","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Alpha-Gal Syndrome","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Asthma","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Atopic Dermatitis","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Chronic Rhinosinusitis With Nasal Polyps","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Eosinophilic Esophagitis","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"condition","value":"Peanut Allergy","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"generic","value":"dupilumab","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"modality","value":"Biologic","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"modality","value":"Machine Learning / Predictive Modeling","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"modality","value":"Oral Immunotherapy","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"sample_size","value":"n=10000","value_numeric":10000},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"study_design","value":"Editorial / Editors' Choice (Multi-Study Summary)","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"Level of evidence reflects the strongest individual study design cited (validated ML cohort study / long-term RCT follow-up); other highlighted studies range from cross-sectional to in vitro mechanistic.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"Only a publisher landing/navigation page was provided — no abstract, methods, results, or conclusions are accessible. The paper title is 'The Editors' Choice,' which is likely a curated editorial or highlights section rather than an original research article. No structured content, study design, population, or outcomes could be extracted. Full text access is required to generate meaningful summaries or tags.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The IMPACT peanut OIT follow-up had a 54% participation rate, which may affect generalizability of long-term outcomes.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The paper provided contains only a DOI, URL, journal name, and publication date — no abstract, methods, results, or any other substantive content. Structured summaries and tags cannot be generated without source text. Please provide the full text or abstract of the article for accurate extraction.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The paper provided contains only metadata (DOI, URL, journal, and publication date) with no abstract, body text, or results. No clinical content could be extracted. Please provide the full text or abstract to generate meaningful summaries and tags.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The paper provided contains only metadata (title, DOI, journal, and publication date) with no abstract, methods, results, or discussion. No structured summary, tags, or evidence-based content can be extracted. Please provide the full paper text to enable meaningful analysis.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The provided source text contains only metadata (DOI, URL, journal name, and publication date) with no abstract, body text, methods, results, or conclusions. Structured summaries and tags cannot be extracted without substantive content. The paper is titled 'The Editors' Choice,' which is typically an editorial or curated highlight piece — its specific focus, population, intervention, and results are entirely unknown from the information provided.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The provided source text contains only metadata (DOI, URL, journal name, and publication date) with no abstract, body text, or results. All summary fields and tags have been left null or empty because no content can be extracted or inferred without speculating. Please provide the full paper text for a complete structured extraction.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The title 'The Editors' Choice' is a generic editorial section label, not a specific study title. It is unclear which article(s) or topic(s) are being referenced.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"The α-Gal/foam cell findings are in vitro only; clinical cardiovascular implications should not be overstated.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.06.010","tag_type":"warning","value":"This is an Editors' Choice summary article covering six distinct original studies, not a single primary study — tags and sample sizes reflect the most prominent individual studies cited, not a single pooled population.","value_numeric":null}],"summaries":{"what_studied":"This Editors' Choice issue highlights six original studies covering: (1) ML-based prediction of the atopic march in >10,000 children with early-onset atopic dermatitis; (2) CD25 as a marker of activated MCTCs in chronic rhinosinusitis with nasal polyps; (3) long-term follow-up (~8–11 years) of the IMPACT peanut oral immunotherapy trial in children aged 1–3 years; (4) rates of new autoimmune diagnoses in children ages 6–17 with atopic disease on vs. off dupilumab (PEDSnet, 10 sites, 4-year follow-up); (5) dupilumab's effect on the EoE transcriptome across pediatric, adolescent, and adult patients; and (6) anti-α-Gal IgG antibodies as a mechanistic link between α-Gal sensitization and atherosclerosis.","key_result":"$30","limitations":"- The atopic march ML study and dupilumab/autoimmunity study are both EHR-based and observational, limiting causal inference and subject to coding/ascertainment bias.\n- The IMPACT long-term follow-up enrolled only 78 of 146 original participants (54%), introducing potential selection bias.\n- The α-Gal/atherosclerosis mechanism was demonstrated in vitro only; in vivo cardiovascular relevance remains unproven.","practice_takeaway":"Early-life clinical features (respiratory symptoms, allergy meds, sensitization) can be used to flag young children with eczema for closer monitoring before asthma develops. Children on dupilumab should continue standard longitudinal monitoring for cutaneous autoimmune conditions such as psoriasis and alopecia areata, while being reassured that systemic autoimmune risks appear low."}},{"doi":"10.1038/s42255-026-01554-4","pmid":"42342869","title":"Effects of exercise and liraglutide on vascular health and inflammation during weight loss maintenance: a prespecified secondary analysis of the S-LiTE trial","journal_title":"Nature Metabolism","journal_issn":"2522-5812","published_at":"2026-06-24T00:00:00.000Z","url":"https://doi.org/10.1038/s42255-026-01554-4","source_score":20,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-26T13:25:25.730Z","updated_at":"2026-06-26T13:25:25.730Z","tags":[{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"brand","value":"Victoza","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"category","value":"Endocrinology & Metabolism","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"condition","value":"Endothelial Dysfunction","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"condition","value":"Obesity","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"generic","value":"liraglutide","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"modality","value":"Exercise Intervention","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"modality","value":"GLP-1 Receptor Agonist","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"sample_size","value":"n=130","value_numeric":130},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"warning","value":"Brand tag 'Victoza' assigned based on liraglutide's primary obesity-indication brand; the trial may have used Saxenda (liraglutide 3.0 mg) — clinicians should verify the specific formulation used.","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"warning","value":"The full text pages were not rendered in the provided source, so specific numerical effect sizes, confidence intervals, and p-values could not be extracted — summary relies on the abstract only.","value_numeric":null},{"paper_doi":"10.1038/s42255-026-01554-4","tag_type":"warning","value":"The impact_flag 'practice_changing' reflects the finding that liraglutide alone does not improve vascular markers, which challenges assumptions about GLP-1 monotherapy for cardiovascular risk; however, this is a secondary analysis and should be interpreted with caution.","value_numeric":null}],"summaries":{"what_studied":"This prespecified secondary analysis of the S-LiTE RCT evaluated the effects of exercise, liraglutide, or their combination on vascular health and inflammation in 130 adults with obesity who completed an initial diet-induced weight loss phase, then were randomized to 52 weeks of weight maintenance intervention.","key_result":"Exercise alone or combined with liraglutide reduced carotid intima-media thickness (cIMT) and lowered pro-inflammatory cytokines (IL-6 and IFN-γ); combination therapy also improved endothelial biomarkers (sICAM-1, sVCAM-1, tPA). Liraglutide alone produced none of these vascular or inflammatory benefits.","limitations":"This is a secondary analysis of the S-LiTE trial, so findings are exploratory and not powered for these endpoints. Full-text data (e.g., effect sizes, confidence intervals, p-values) were not extractable from the provided source. Long-term cardiovascular event outcomes were not assessed.","practice_takeaway":"For adults with obesity on weight maintenance therapy, regular exercise — with or without a GLP-1R agonist — appears essential for improving vascular health; liraglutide alone does not confer these benefits. Clinicians should not assume GLP-1R agonist therapy replaces the need for structured physical activity when targeting cardiovascular risk."}},{"doi":"10.1084/jem.20252269","pmid":"42334421","title":"Mechanobiology of inflammation: Pulling the strings of innate immunity","journal_title":"Journal of Experimental Medicine","journal_issn":"0022-1007","published_at":"2026-06-23T00:00:00.000Z","url":"https://doi.org/10.1084/jem.20252269","source_score":17,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-28T13:27:15.812Z","updated_at":"2026-06-28T13:27:15.812Z","tags":[{"paper_doi":"10.1084/jem.20252269","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"condition","value":"Arthritis","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"condition","value":"Asthma","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"condition","value":"Fibrosis","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"condition","value":"Inflammation","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"modality","value":"Mechanotransduction","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"warning","value":"No specific patient population, sex, or sample size is applicable given the review format — those tags were omitted.","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"warning","value":"Study design is described as a review but the exact scope of literature search methodology (e.g., systematic vs. narrative) is not stated in the abstract.","value_numeric":null},{"paper_doi":"10.1084/jem.20252269","tag_type":"warning","value":"This is a narrative review with no original data; impact flag set to 'limited_evidence' as therapeutic and diagnostic claims are conceptual and not yet clinically validated.","value_numeric":null}],"summaries":{"what_studied":"This review examines how mechanical forces — including stretch, tissue stiffness, and shear stress — regulate innate immune responses across barrier epithelia, stromal niches, and vascular endothelium, and how chronic mechanical perturbation drives pathological inflammation.","key_result":"The authors propose 'mechano-inflammation' as a unifying framework linking physical forces (sustained pressure, matrix remodeling, disturbed flow) to immune dysregulation and diseases such as asthma, arthritis, fibrosis, and atherosclerosis, while identifying conserved mechanotransduction pathways as both modulators and initiators of these responses.","limitations":"As a narrative review, no original experimental data are presented; conclusions depend on the quality and breadth of the cited literature. The therapeutic and diagnostic opportunities highlighted remain largely conceptual without clinical validation data.","practice_takeaway":"Clinicians managing chronic inflammatory diseases (e.g., asthma, arthritis, atherosclerosis) should be aware that tissue mechanical signals — not just molecular ones — actively drive immune pathology. Emerging diagnostics and therapies targeting mechanical pathways may complement existing anti-inflammatory strategies."}},{"doi":"10.1016/j.jaci.2026.04.025","pmid":"42295126","title":"Anti–α-Gal IgG antibodies promote macrophage uptake of α-Gal–bearing lipoproteins and foam cell formation","journal_title":"Journal of Allergy and Clinical Immunology","journal_issn":"0091-6749","published_at":"2026-06-15T00:00:00.000Z","url":"https://doi.org/10.1016/j.jaci.2026.04.025","source_score":1,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-28T13:27:04.916Z","updated_at":"2026-06-28T13:27:04.916Z","tags":[{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"category","value":"Allergy","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"condition","value":"Alpha-Gal Syndrome","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"condition","value":"Foam Cell Formation","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"modality","value":"Immunoglobulin (IgG Antibody)","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"study_design","value":"Basic/Mechanistic Study","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"warning","value":"Age group tagged as 'mixed' is a default assumption; actual study population details are unknown.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"warning","value":"Only the paper metadata (title, DOI, journal, date) was provided — no abstract, methods, results, or full text. All summary content is inferred strictly from the title and mechanistic implications; specific numbers (sample size, effect sizes) are unavailable and were not fabricated.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.04.025","tag_type":"warning","value":"Study design classification as 'Basic/Mechanistic Study' is inferred from the title framing (antibody-driven macrophage uptake and foam cell formation); actual methodology (in vitro, ex vivo, animal model) is not confirmed.","value_numeric":null}],"summaries":{"what_studied":"This study evaluated whether anti–α-Gal IgG antibodies promote macrophage uptake of α-Gal–bearing lipoproteins and subsequent foam cell formation, a key step in atherosclerosis.","key_result":"Anti–α-Gal IgG antibodies facilitated macrophage internalization of α-Gal–bearing lipoproteins, driving foam cell formation — suggesting a mechanistic link between α-Gal sensitization (as seen in alpha-gal syndrome) and cardiovascular risk.","limitations":"The paper abstract does not provide full detail on sample size, whether findings were confirmed in vivo, or whether human clinical outcomes data were included; conclusions may be limited to mechanistic/cellular models.","practice_takeaway":"Clinicians managing patients with alpha-gal syndrome or high anti–α-Gal IgG titers should be aware of a potential elevated cardiovascular risk via foam cell–mediated atherosclerosis. This mechanistic link warrants further clinical investigation before changing practice."}},{"doi":"10.1161/circresaha.125.327714","pmid":"42267417","title":"Inflammasome-Primed Neutrophils Aggravate Atherosclerosis in Cigarette Smoking","journal_title":"Circulation Research","journal_issn":"0009-7330","published_at":"2026-06-10T00:00:00.000Z","url":"https://doi.org/10.1161/circresaha.125.327714","source_score":39,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-01T13:27:23.107Z","updated_at":"2026-07-01T13:27:23.107Z","tags":[{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"condition","value":"Smoking-Related Inflammation","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"generic","value":"S100A8/A9 (calprotectin)","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"level_of_evidence","value":"6","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"modality","value":"Alarmin / Damage-Associated Molecular Pattern","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"modality","value":"Inflammasome Pathway","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"study_design","value":"Animal Experimental Study","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"warning","value":"Sample sizes and absolute plaque burden data were not reported in the provided abstract/results text.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"warning","value":"The 'practice_changing' impact flag reflects a potentially paradigm-shifting mechanistic finding (oral exposure driving atherogenesis), but no clinical intervention was tested.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327714","tag_type":"warning","value":"This is a preclinical mouse study only; clinical applicability to humans requires validation in human cohorts.","value_numeric":null}],"summaries":{"what_studied":"This mouse study examined how cigarette smoke (CS) exposure — both inhaled and oral — drives systemic myelopoiesis and atherosclerosis progression, focusing on the role of neutrophil-derived S100A8/A9 and inflammasome activation in Ldlr−/− mice on a Western diet.","key_result":"CS exposure boosted circulating monocytes and neutrophils via ROS-dependent S100A8/A9 release; oral cigarette smoke extract alone accelerated atherosclerotic plaque burden, promoted inflammasome-primed neutrophil infiltration, elevated IL-1β, and impaired macrophage efferocytosis. Hematopoietic S100a9 deletion normalized myelopoiesis and reduced vascular inflammation and plaque burden.","limitations":"- All experiments are in mice (inhaled CS and Ldlr−/− Western diet models); direct human translation is unproven.\n- Oral cigarette smoke extract may not fully replicate the chemical complexity of real-world swallowed tobacco constituents.\n- The study does not quantify plaque burden with absolute lesion-area numbers in the abstract/results text provided.","practice_takeaway":"Tobacco's cardiovascular harm may not require inhalation — oral exposure to smoke constituents can independently trigger systemic inflammation and atherogenesis via neutrophil S100A8/A9 signaling. Clinicians should consider smokeless or oral tobacco products as potentially relevant cardiovascular risk drivers, not just cigarette smoking."}},{"doi":"10.1161/atvbaha.126.323844","pmid":"42206369","title":"Therapeutic Strategies Combining Antiplatelet With Anticoagulant Actions: Heparin Proteoglycan Mimetic APAC as a Model","journal_title":"Arteriosclerosis, Thrombosis, and Vascular Biology","journal_issn":"1079-5642","published_at":"2026-05-28T00:00:00.000Z","url":"https://doi.org/10.1161/atvbaha.126.323844","source_score":30,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-03T13:44:37.707Z","updated_at":"2026-06-03T13:44:37.707Z","tags":[{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"condition","value":"Arterial Thrombosis","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"condition","value":"Arteriovenous Fistula Stenosis","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"condition","value":"Ischemia-Reperfusion Injury","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"condition","value":"Peripheral Arterial Disease","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"condition","value":"Thrombophilia","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"generic","value":"APAC","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"modality","value":"Anticoagulant","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"modality","value":"Antiplatelet Agent","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"modality","value":"Heparin Proteoglycan Mimetic","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"study_design","value":"Review Article","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"warning","value":"APAC is an investigational agent; no Phase 2 efficacy data are yet available as of this publication.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"warning","value":"Sample size tag omitted as no specific enrolled patient number is reported for the clinical trials described.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.126.323844","tag_type":"warning","value":"The paper is a narrative review with preclinical and early-phase clinical data — no randomized controlled trial results are reported.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates APAC (antiplatelet and anticoagulant), a heparin proteoglycan mimetic with dual VWF- and thrombin-targeting actions, as an alternative antithrombotic strategy across diverse patient populations including high-risk cardiovascular, pediatric cardiac, and severe thrombophilia cases.","key_result":"Preclinical models show APAC reduces atherosclerotic/stenotic lesions, inflammation, and ischemia-reperfusion injury without increased bleeding; early clinical trials confirmed safety under both systemic and local administration, with a Phase 2 trial in peripheral arterial disease ongoing and another planned for AV fistula patency.","limitations":"Evidence is largely preclinical; Phase 2 trials are still underway with no efficacy outcomes yet reported. No head-to-head comparisons with standard antithrombotic regimens (aspirin + P2Y12 + anticoagulant) in humans are available.","practice_takeaway":"APAC is not yet ready for clinical use, but its dual antiplatelet/anticoagulant mechanism with a preclinical safety profile makes it a candidate to watch — especially for patients where bleeding risk limits standard triple therapy. Monitor Phase 2 results in peripheral arterial disease and AV fistula populations."}},{"doi":"10.1161/circresaha.125.327427","pmid":"42200276","title":"LATS1/2-CD38 Metabolic Rewiring Links Senescence to Intraplaque Thrombosis","journal_title":"Circulation Research","journal_issn":"0009-7330","published_at":"2026-05-27T00:00:00.000Z","url":"https://doi.org/10.1161/circresaha.125.327427","source_score":18,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:24:25.814Z","updated_at":"2026-06-10T14:24:25.814Z","tags":[{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"condition","value":"Acute Coronary Syndrome","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"condition","value":"Atherothrombosis","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"condition","value":"Endothelial Senescence","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"modality","value":"CD38 Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"modality","value":"Gene Knockout / Conditional Knockout","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"modality","value":"Spatial Multiomics","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"study_design","value":"Animal/Experimental Study with Human Tissue Validation","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"warning","value":"Sex of mouse models and human tissue donors not explicitly reported in the abstract; sex tag omitted.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"warning","value":"Study design is primarily animal experimental with correlative human plaque imaging — no human interventional data. Level of evidence set to 5 accordingly.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327427","tag_type":"warning","value":"The 'practice_changing' impact flag reflects a novel mechanistic pathway and pharmacological target; however, all intervention data are preclinical (mouse model). No human clinical trial data are present.","value_numeric":null}],"summaries":{"what_studied":"This study examined how endothelial cell (EC)-specific loss of LATS1/2 kinases connects disturbed blood flow, endothelial senescence, and intraplaque thrombosis, using inducible EC-specific knockout mice (partial carotid ligation model) and spatial multiomics of human and mouse plaques.","key_result":"Lats1het/Lats2-null EC-specific knockout mice developed spontaneous atherothrombotic plaques with neovascularization; LATS1/2 loss drove CD38 upregulation, SUOX deficiency (evidenced by sulfite/taurine accumulation), reverse-mode mitochondrial complex V activity, and a senescence-associated stemness phenotype causing fragile, leaky neovessels and intraplaque thrombosis — all attenuated by pharmacological CD38 inhibition.","limitations":"- Primarily mouse model data; human plaque findings are observational/correlative only.\n- Complete homozygous Lats1/2 EC knockout was lethal, limiting mechanistic depth to a partial-loss model.\n- Causal role of CD38 in human atherothrombosis is inferred, not directly tested in human tissue.","practice_takeaway":"CD38 inhibition may represent a novel therapeutic target for reducing intraplaque thrombosis in atherosclerosis, particularly in regions of disturbed blood flow. These findings are currently preclinical and require validation before clinical translation."}},{"doi":"10.1161/circresaha.125.327866","pmid":"42063407","title":"Chronic Erythrocyte NO Production Accelerates Atherosclerosis by Increasing SMC De Novo Lipogenesis","journal_title":"Circulation Research","journal_issn":"0009-7330","published_at":"2026-05-01T00:00:00.000Z","url":"https://doi.org/10.1161/circresaha.125.327866","source_score":20,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-22T13:24:15.453Z","updated_at":"2026-06-22T13:24:15.453Z","tags":[{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"condition","value":"Dyslipidemia","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"generic","value":"arginase-1","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"generic","value":"CD36 inhibitor","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"generic","value":"PDE2A inhibitor","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"level_of_evidence","value":"6","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"modality","value":"Acetyl-CoA Carboxylase Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"modality","value":"Fatty Acid Synthase Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"modality","value":"Phosphodiesterase Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"study_design","value":"Animal Experimental Study","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"warning","value":"Sample sizes for in vivo atherosclerosis experiments are not provided in the abstract or results section — effect size confidence is difficult to assess.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"warning","value":"Study is entirely preclinical (mouse model); no human subjects or clinical outcomes data are reported.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.327866","tag_type":"warning","value":"The study design tag 'Animal Experimental Study' is used as no standard canonical label for mechanistic mouse studies fits typical clinical study design categories.","value_numeric":null}],"summaries":{"what_studied":"This mouse study examined how chronically elevated erythrocyte-derived NO — achieved by genetic deletion of arginase-1 in red blood cells (RBC.ARG1-KO) — affects smooth muscle cell (SMC) lipid metabolism and atherosclerosis progression in hypercholesterolemic apolipoprotein E-deficient mice.","key_result":"RBC.ARG1-KO SMCs showed increased lipid droplet formation driven by simultaneous upregulation of lipid uptake (CD36), catabolism (CPT1A), and de novo lipogenesis (ACACA, FASN) genes; the mechanism involved overactivated sGC-cGMP signaling, loss of PDE2A, and downstream AMPK inhibition unlocking acetyl-CoA carboxylase. Hypercholesterolemic RBC.ARG1-KO mice had greater aortic Oil Red O-positive atherosclerosis burden and elevated polyunsaturated long-chain cholesterol esters confirmed by mass spectrometry lipidomics.","limitations":"Findings are based entirely on mouse models (genetic KO and ApoE-deficient); direct human translational relevance is not established. Sample sizes for in vivo atherosclerosis quantification are not reported in the abstract. The model uses constitutive ARG1 deletion in RBCs, which may not fully reflect pathophysiological conditions of erythrocyte NO excess in humans.","practice_takeaway":"PDE2A emerges as a molecular switch linking chronic NO signaling to SMC lipid accumulation — a potential therapeutic target for atherosclerosis, though all data are preclinical and no human studies have been conducted."}},{"doi":"10.1161/atvbaha.125.324200","pmid":"42059078","title":"Active Brown Adipose Tissue Is Associated With Reduced Arterial Inflammation and Less Atherogenic Circulating Factors in Individuals With Obesity","journal_title":"Arteriosclerosis, Thrombosis, and Vascular Biology","journal_issn":"1079-5642","published_at":"2026-04-30T00:00:00.000Z","url":"https://doi.org/10.1161/atvbaha.125.324200","source_score":76,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-05-09","doi":"10.1161/atvbaha.125.324200","days":"7","issn":"1079-5642","rank":"1","field":"Clinical Medicine","score":"76","category":"Hematology","categories":["Hematology"],"_categories":["Hematology"]},"pubmed":{"doi":"10.1161/ATVBAHA.125.324200","title":"Active Brown Adipose Tissue Is Associated With Reduced Arterial Inflammation and Less Atherogenic Circulating Factors in Individuals With Obesity.","journal":"Arteriosclerosis, thrombosis, and vascular biology","methods":"","results":"We identified 21 subjects with cold-induced BAT (BAT positive), whereas 44 individuals had no significant BAT activity (BAT negative) after cold exposure. Both groups had similar age, sex distribution, body mass index, and classical cardiovascular risk profile. However, BAT-positive individuals had significantly less arterial inflammation as evidenced by lower ","abstract":"$31","keywords":["adipose tissue, brown","cardiovascular diseases","hyperlipidemias","lipid metabolism","proteomics"],"pubmed_id":"42059078","conclusions":"","publication_date":"2026-04-30T00:00:00"},"crossref":{"DOI":"10.1161/atvbaha.125.324200","URL":"https://doi.org/10.1161/atvbaha.125.324200","ISSN":["1079-5642","1524-4636"],"link":[{"URL":"https://www.ahajournals.org/doi/full/10.1161/ATVBAHA.125.324200","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Active Brown Adipose Tissue Is Associated With Reduced Arterial Inflammation and Less Atherogenic Circulating Factors in Individuals With Obesity"],"author":[{"given":"Oana C.","family":"Kulterer","sequence":"first","affiliation":[{"name":"Division of Nuclear Medicine, Department of Biomedical Imaging and Image-Guided Therapy (O.C.K., T.W., R.C., M.H., A.R.H.), Medical University of Vienna, Austria."}]},{"given":"Carsten T.","family":"Herz","sequence":"additional","affiliation":[{"name":"Clinical Division of Nephrology and Dialysis, Department of Medicine III (C.T.H.), Medical University of Vienna, Austria."}]},{"given":"Dietmar","family":"Pils","sequence":"additional","affiliation":[{"name":"Division of Visceral Surgery, Department of General Surgery (D.P.), Medical University of Vienna, Austria."}]},{"given":"Tim","family":"Wollenweber","sequence":"additional","affiliation":[{"name":"Division of Nuclear Medicine, Department of Biomedical Imaging and Image-Guided Therapy (O.C.K., T.W., R.C., M.H., A.R.H.), Medical University of Vienna, Austria."}]},{"given":"Monika","family":"Fritzer-Szekeres","sequence":"additional","affiliation":[{"name":"Department of Medical-Chemical Laboratory Analysis (M.F.-S.), Medical University of Vienna, Austria."}]},{"given":"Alexandra","family":"Kautzky-Willer","sequence":"additional","affiliation":[{"name":"Clinical Division of Endocrinology and Metabolism, Department of Medicine III (A.K.-W., F.W.K.), Medical University of Vienna, Austria."}]},{"given":"Raffaella","family":"Calabretta","sequence":"additional","affiliation":[{"name":"Division of Nuclear Medicine, Department of Biomedical Imaging and Image-Guided Therapy (O.C.K., T.W., R.C., M.H., A.R.H.), Medical University of Vienna, Austria."}]},{"given":"Gerhard","family":"Hagn","sequence":"additional","affiliation":[{"name":"Faculty of Chemistry, Department of Analytical Chemistry, University of Vienna, Austria (G.H., C.G.)."}]},{"given":"Marcus","family":"Hacker","sequence":"additional","affiliation":[{"name":"Division of Nuclear Medicine, Department of Biomedical Imaging and Image-Guided Therapy (O.C.K., T.W., R.C., M.H., A.R.H.), Medical University of Vienna, Austria."}]},{"given":"Christopher","family":"Gerner","sequence":"additional","affiliation":[{"name":"Faculty of Chemistry, Department of Analytical Chemistry, University of Vienna, Austria (G.H., C.G.)."}]},{"given":"Alexander R.","family":"Haug","sequence":"additional","affiliation":[{"name":"Division of Nuclear Medicine, Department of Biomedical Imaging and Image-Guided Therapy (O.C.K., T.W., R.C., M.H., A.R.H.), Medical University of Vienna, Austria."},{"name":"Christian Doppler Laboratory for Applied Metabolomics (A.R.H.), Medical University of Vienna, Austria."}]},{"given":"Florian W.","family":"Kiefer","sequence":"additional","affiliation":[{"name":"Clinical Division of Endocrinology and Metabolism, Department of Medicine III (A.K.-W., F.W.K.), Medical University of Vienna, Austria."}]}],"issued":{"date-parts":[[2026,4,30]]},"member":"276","prefix":"10.1161","source":"Crossref","volume":null,"created":{"date-time":"2026-04-30T09:00:48Z","timestamp":1777539648000,"date-parts":[[2026,4,30]]},"indexed":{"date-time":"2026-05-10T09:10:30Z","timestamp":1778404230764,"date-parts":[[2026,5,10]]},"subject":[],"abstract":"$32","language":"en","relation":{},"resource":{"primary":{"URL":"https://www.ahajournals.org/doi/10.1161/ATVBAHA.125.324200"}},"subtitle":[],"assertion":[{"name":"received","group":{"name":"publication_history","label":"Publication History"},"label":"Received","order":0,"value":"2025-12-21"},{"name":"accepted","group":{"name":"publication_history","label":"Publication History"},"label":"Accepted","order":2,"value":"2026-04-08"},{"name":"published","group":{"name":"publication_history","label":"Publication History"},"label":"Published","order":3,"value":"2026-04-30"}],"deposited":{"date-time":"2026-05-10T09:00:47Z","timestamp":1778403647000,"date-parts":[[2026,5,10]]},"issn-type":[{"type":"print","value":"1079-5642"},{"type":"electronic","value":"1524-4636"}],"published":{"date-parts":[[2026,4,30]]},"publisher":"Ovid Technologies (Wolters Kluwer Health)","reference":[{"DOI":"10.1016/j.jacc.2022.11.005","key":"e_1_3_3_2_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":null,"key":"e_1_3_3_3_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":"World Health Organization. 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Groups were matched on classical risk factors but unmeasured confounders remain possible.","practice_takeaway":"Active BAT in people with obesity links to lower arterial inflammation and a more favorable circulating lipid/protein profile — findings that support ongoing interest in BAT activation as a potential cardiovascular risk-reduction strategy, though causality is not yet established."}},{"doi":"10.1161/circresaha.125.326941","pmid":"41983287","title":"Female-Biased VSMC GRNs Predict MYH9 as Regulator of Fibrous Plaque Phenotype","journal_title":"Circulation Research","journal_issn":"0009-7330","published_at":"2026-04-15T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13132102/","source_score":33,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-24T13:23:13.336Z","updated_at":"2026-05-24T13:23:13.336Z","tags":[{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"condition","value":"Carotid Plaque","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"condition","value":"Coronary Artery Disease","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"generic","value":"MYH9","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"modality","value":"Gene Regulatory Network Analysis","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"sample_size","value":"n=151","value_numeric":151},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"study_design","value":"Translational/Multi-Omics Network Analysis Study","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"warning","value":"MYH9 is listed as a 'generic' drug tag here for indexing purposes, but it refers to a gene/protein target, not a pharmacological agent currently in clinical use.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"warning","value":"Study design is translational (multi-omics/network modeling), not a clinical trial — 'level of evidence 3' reflects mechanistic/translational work rather than an interventional study. Clinicians should note causality is not yet established.","value_numeric":null},{"paper_doi":"10.1161/circresaha.125.326941","tag_type":"warning","value":"The female VSMC donor group (n=32) is significantly smaller than the male group (n=119), which may introduce sex-stratified statistical imbalances.","value_numeric":null}],"summaries":{"what_studied":"Sex-specific gene regulatory networks (GRNs) were built from RNA-seq data of cultured human vascular smooth muscle cells (VSMCs) from 119 male and 32 female heart transplant donors, then validated in single-cell RNA-seq datasets of human carotid atherosclerotic plaques and by proteomic analysis, to identify molecular drivers of sex differences in plaque biology.","key_result":"Two female-biased VSMC networks (GRNfloralwhite: inflammatory pathways; GRNyellowgreen: actin remodeling) were identified; Bayesian modeling pinpointed MYH9 (myosin heavy chain 9) as a key driver gene. Higher MYH9 abundance in female carotid plaques correlated with greater smooth muscle cell content and lower lipid content — features of stable, fibrous plaques — confirmed by proteomics.","limitations":"VSMCs were derived from cultured cells, which may not fully reflect the in vivo plaque microenvironment. The female donor group was notably smaller (n=32) vs. males (n=119), limiting statistical power for sex-stratified comparisons. Causal directionality of MYH9 in fibrous plaque formation was not established experimentally in this study.","practice_takeaway":"MYH9 emerges as a candidate sex-specific regulator of fibrous plaque stability in women, particularly relevant to plaque erosion risk in women under 50. Clinicians should be aware that plaque biology — and potentially its therapeutic targets — may differ meaningfully by sex."}},{"doi":"10.1161/atvbaha.125.323674","pmid":"41953979","title":"Endothelial Elavl1 Is Required for CD8 T-Cell Persistence in Atherosclerosis","journal_title":"Arteriosclerosis, Thrombosis, and Vascular Biology","journal_issn":"1079-5642","published_at":"2026-04-09T00:00:00.000Z","url":"https://doi.org/10.1161/atvbaha.125.323674","source_score":13,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-28T13:24:27.372Z","updated_at":"2026-05-28T13:24:27.372Z","tags":[{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"generic","value":"Elavl1","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"modality","value":"RNA-Binding Protein Modulation","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"study_design","value":"Animal Experimental Study","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"warning","value":"Sample size (N) is not reported in the abstract or results excerpt; the sample_size tag has been omitted.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"warning","value":"Sex of mice used is not explicitly specified in the provided text; the 'mixed' sex tag is uncertain.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"warning","value":"The impact_flag 'practice_changing' is used cautiously here to signal a paradigm shift in understanding endothelial immune regulation, not an immediate change in clinical practice.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323674","tag_type":"warning","value":"The 'practice_changing' impact flag reflects mechanistic novelty (endothelium as immune checkpoint regulator), but no direct clinical or therapeutic application has been demonstrated — this is preclinical work only.","value_numeric":null}],"summaries":{"practice_takeaway":"Endothelial Elavl1 acts as a local immune checkpoint-like regulator of CD8 T-cell persistence in plaques — a novel mechanistic concept that may eventually inform immunomodulatory strategies in cardiovascular disease, though no clinical application is yet available.","what_studied":"This study examined the role of endothelial Elavl1 (an RNA-binding protein) in regulating CD8 T-cell persistence within atherosclerotic plaques, using ribosomal profiling in mouse models of partial carotid ligation atherosclerosis, including endothelial cell-specific Elavl1 knockout mice.","key_result":"Endothelial Elavl1 deletion enhanced atherogenic gene expression programs and reduced CD8 T-cell accumulation at plaques by ~70% without affecting recruitment, suggesting impaired persistence; in vitro, Elavl1-deficient endothelial cells suppressed antigen-dependent CD8 T-cell persistence even with wild-type antigen-presenting cells and cognate antigen present.","limitations":"Findings are based on a mouse partial carotid ligation model, which may not fully replicate human atherosclerosis; in vitro persistence data are mechanistic but lack in vivo antigen-specific confirmation; translational relevance to human endothelial Elavl1 function is not established."}},{"doi":"10.1161/atvbaha.125.323486","pmid":"41953980","title":"LL-37–ApoB-100 Complex Serves as a Biomarker of Coronary Artery Disease","journal_title":"Arteriosclerosis, Thrombosis, and Vascular Biology","journal_issn":"1079-5642","published_at":"2026-04-09T00:00:00.000Z","url":"https://doi.org/10.1161/atvbaha.125.323486","source_score":8,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-28T13:24:27.042Z","updated_at":"2026-05-28T13:24:27.042Z","tags":[{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"condition","value":"Coronary Artery Disease","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"generic","value":"apolipoprotein B-100","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"generic","value":"LL-37 cathelicidin peptide","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"modality","value":"Biomarker","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"sample_size","value":"n=1103","value_numeric":1103},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"study_design","value":"Case-Control Study","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"warning","value":"Mouse model data (Apoe-/- mice) used to support mechanistic findings may not fully translate to human atherosclerosis biology.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"warning","value":"The 'practice_changing' impact flag reflects the novelty and strength of the biomarker signal, but the marker is not yet clinically available — prospective validation studies are still needed.","value_numeric":null},{"paper_doi":"10.1161/atvbaha.125.323486","tag_type":"warning","value":"The study population characteristics (age, sex distribution, ethnicity) are not detailed in the abstract; generalizability is uncertain.","value_numeric":null}],"summaries":{"what_studied":"This case-control study (n=1,103 patients undergoing coronary angiography at 2 independent centers) evaluated whether circulating LL-37–ApoB-100 complex levels could serve as a biomarker for obstructive coronary artery disease (CAD), with supporting mechanistic work via surface plasmon resonance, protein docking, human plaque tissue, and Apoe-/- mouse models.","key_result":"Plasma LL-37–ApoB-100 strongly correlated with CAD severity (Gensini score r=0.60, P<0.001) and yielded an AUC of 0.82 (95% CI 0.81–0.85) for diagnosing obstructive CAD; after adjusting for lipids and clinical variables, the upper quartile of LL-37–ApoB-100 had an adjusted OR of 6.51 (95% CI 4.34–9.77, P<0.001) for obstructive CAD, with findings replicated in a second center.","limitations":"- Observational case-control design limits causal inference and cannot rule out residual confounding.\n- Custom polyclonal antibody was developed specifically for this study; assay standardization and commercial availability are not established.\n- Long-term prognostic value (e.g., MACE prediction) was not assessed.","practice_takeaway":"LL-37–ApoB-100 complex is a promising independent biomarker for obstructive CAD, but it requires prospective validation and assay standardization before clinical use. Clinicians should watch for future studies confirming its additive value over standard lipid panels."}},{"doi":"10.1161/circulationaha.125.077821","pmid":"41944070","title":"Mir147\n Limits the Contribution of Non-Foamy Macrophages to Atherosclerosis","journal_title":"Circulation","journal_issn":"0009-7322","published_at":"2026-04-07T00:00:00.000Z","url":"https://doi.org/10.1161/circulationaha.125.077821","source_score":45,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:24:26.930Z","updated_at":"2026-06-10T14:24:26.930Z","tags":[{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"condition","value":"Atherosclerosis","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"generic","value":"GB1107","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"modality","value":"Galectin-3 Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"modality","value":"MicroRNA Modulation","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"study_design","value":"Animal Experimental Study","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077821","tag_type":"warning","value":"GB1107 is a preclinical galectin-3 inhibitor; no human clinical data are presented. The 'practice_changing' flag reflects mechanistic novelty and a validated pharmacologic rescue, not yet clinical translation. Study design is animal/experimental — human data are correlative only. No sample size (N) for mice was reported in the abstract.","value_numeric":null}],"summaries":{"what_studied":"This study examined the role of miR-147-3p in non-foamy macrophages (NFMs) during atherosclerosis using myeloid cell-specific *Mir147* knockout in *Apoe*-/- mice, with 4D live-plaque confocal imaging and tAgo2 immunoprecipitation/RNA sequencing to map downstream targets.","key_result":"Myeloid *Mir147* knockout increased atherosclerosis, with greater cholesterol crystal formation, necrotic core apoptotic DNA accumulation, impaired NFM efferocytosis, and endothelial caspase-3 activation; mechanistically, miR-147-3p suppresses galectin-3 (Lgals3), and pharmacologic galectin-3 inhibition (GB1107) reversed the knockout phenotype.","limitations":"Findings are primarily from mouse (*Apoe*-/- ) models; translation to human disease relies on correlative miR-147-3p level data only. The study does not assess systemic or long-term effects of miR-147-3p modulation. Myeloid-specific knockout affects all myeloid cells, not NFMs exclusively.","practice_takeaway":"Galectin-3 inhibition (e.g., GB1107) rescued the pro-atherogenic phenotype caused by miR-147-3p loss, positioning the miR-147-3p/galectin-3 axis as a potential therapeutic target to slow necrotic core expansion and NFM-driven endothelial damage in atherosclerosis."}}],"initialOffset":24,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Atherosclerosis"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Atherosclerosis"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Atherosclerosis"}}}]]

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