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:T766,Cardiovascular events are major determinants of morbidity and mortality in systemic lupus erythematosus (SLE), particularly in patients with renal involvement. Although oxidative stress has been implicated in driving vascular and renal damage in SLE, the specific mechanisms remain unclear. This study investigated the potential role of oxidative stress-induced alterations in fibrinogen structure and function in the pathogenesis of atherothrombosis in SLE. In this cross-sectional study, we enrolled 144 adult patients with SLE and 90 matched controls. We measured blood leukocyte reactive oxygen species (ROS) production, systemic redox status, and the structural and functional features of purified fibrinogen. Correlations between these parameters and disease activity were also investigated. In vitro experiments to clarify the causal relationships among ROS levels, protein oxidation, and fibrin abnormalities provided mechanistic insights of the observed alterations. Patients with SLE showed increased leukocyte ROS production, mainly due to neutrophil NADPH oxidase activation. Interestingly, renal biopsies from patients with SLE with active proliferative lupus nephritis exhibited overexpression of the NADPH oxidase enzyme complex p22phox. This was accompanied by plasma oxidative stress as indicated by elevated plasma lipid peroxidation and reduced antioxidant defenses. Fibrinogen oxidation was associated with structural and functional changes, leading to the formation of denser fibrin networks with lower clot porosity and reduced susceptibility to plasmin-mediated fibrin lysis. Interestingly, these fibrinogen modifications correlated with alterations in redox status and disease activity. Oxidative stress may drive structural and functional modifications of fibrinogen in SLE, potentially acting as a novel pathogenetic mechanism in atherothrombosis among these patients.31:T9b3, Objective Cardiovascular events are major determinants of morbidity and mortality in systemic lupus erythematosus (SLE), particularly in patients with renal involvement. Although oxidative stress has been implicated in driving vascular and renal damage in SLE, the specific mechanisms remain unclear. This study investigated the potential role of oxidative stress‐induced alterations in fibrinogen structure and function in the pathogenesis of atherothrombosis in SLE. Methods In this cross‐sectional study, we enrolled 144 adult patients with SLE and 90 matched controls. We measured blood leukocyte reactive oxygen species (ROS) production, systemic redox status, and the structural and functional features of purified fibrinogen. Correlations between these parameters and disease activity were also investigated. In vitro experiments to clarify the causal relationships among ROS levels, protein oxidation, and fibrin abnormalities provided mechanistic insights of the observed alterations. Results Patients with SLE showed increased leukocyte ROS production, mainly due to neutrophil NADPH oxidase activation. Interestingly, renal biopsies from patients with SLE with active proliferative lupus nephritis exhibited overexpression of the NADPH oxidase enzyme complex p22phox. This was accompanied by plasma oxidative stress as indicated by elevated plasma lipid peroxidation and reduced antioxidant defenses. Fibrinogen oxidation was associated with structural and functional changes, leading to the formation of denser fibrin networks with lower clot porosity and reduced susceptibility to plasmin‐mediated fibrin lysis. Interestingly, these fibrinogen modifications correlated with alterations in redox status and disease activity. Conclusion Oxidative stress may drive structural and functional modifications of fibrinogen in SLE, potentially acting as a novel pathogenetic mechanism in atherothrombosis among these patients. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Atherothrombosis: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Atherothrombosis (condition). Clinician-written summaries and actionable practice insights. 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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":"10.1002/art.43371","pmid":"40897511","title":"Reactive Oxygen Species–Induced Modifications of Fibrin Clots as a Link Between Immune Responses and Atherothrombosis in Systemic Lupus Erythematosus","journal_title":"Arthritis & Rheumatology","journal_issn":"2326-5191","published_at":"2025-09-03T00:00:00.000Z","url":"https://doi.org/10.1002/art.43371","source_score":24,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2025-12-31","doi":"10.1002/art.43371","days":"30","issn":"2326-5191","rank":"3","field":"Clinical Medicine","score":"24","category":"Rheumatology","categories":["Rheumatology"],"_categories":["Rheumatology"]},"pubmed":{"doi":"10.1002/art.43371","title":"Reactive Oxygen Species-Induced Modifications of Fibrin Clots as a Link Between Immune Responses and Atherothrombosis in Systemic Lupus Erythematosus.","journal":"Arthritis & rheumatology (Hoboken, N.J.)","methods":"","results":"Patients with SLE showed increased leukocyte ROS production, mainly due to neutrophil NADPH oxidase activation. Interestingly, renal biopsies from patients with SLE with active proliferative lupus nephritis exhibited overexpression of the NADPH oxidase enzyme complex p22phox. This was accompanied by plasma oxidative stress as indicated by elevated plasma lipid peroxidation and reduced antioxidant defenses. Fibrinogen oxidation was associated with structural and functional changes, leading to the formation of denser fibrin networks with lower clot porosity and reduced susceptibility to plasmin-mediated fibrin lysis. Interestingly, these fibrinogen modifications correlated with alterations in redox status and disease activity.","abstract":"$30","keywords":[],"pubmed_id":"40897511","conclusions":"Oxidative stress may drive structural and functional modifications of fibrinogen in SLE, potentially acting as a novel pathogenetic mechanism in atherothrombosis among these patients.","publication_date":"2025-09-03T00:00:00"},"crossref":{"DOI":"10.1002/art.43371","URL":"https://doi.org/10.1002/art.43371","ISSN":["2326-5191","2326-5205"],"link":[{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/art.43371","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Reactive Oxygen Species–Induced Modifications of Fibrin Clots as a Link Between Immune Responses and Atherothrombosis in Systemic Lupus 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fibrinogen structure/function, with correlations to disease activity; in vitro experiments probed ROS-driven fibrinogen oxidation.","key_result":"SLE patients had higher leukocyte ROS driven mainly by neutrophil NADPH oxidase, overexpression of p22phox in renal biopsies of active proliferative lupus nephritis, elevated plasma lipid peroxidation, and reduced antioxidant defenses. 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