This study characterized synovial telocytes in mouse and human joints using scRNA-seq, immunohistochemistry, and in vitro assays — evaluating their marker genes, osmotic stress responses, and capacity to transition into fibroblasts/myofibroblasts in the context of rheumatoid arthritis (RA).
Synovial telocytes are specifically marked by *Efhd1*, *Dpp4*, and *Pi16* (distinct from fibroblast markers *Comp*, *Dkk3*, *Cdh11*), are CD34+/Comp-, reside primarily in the sublining, and are depleted in TNF-induced arthritis. In vitro, telocytes showed greater sensitivity to osmotic pressure than fibroblasts (with a unique mitoflash response) and converted to a myofibroblast phenotype when exposed to a stiff matrix.
Mechanistic in vitro findings rely on mouse-derived telocytes and may not fully translate to human RA pathophysiology. TNF-transgenic mice model chronic TNF-driven inflammation but may not capture the full spectrum of RA. The clinical significance of telocyte-to-myofibroblast transition in human disease remains undemonstrated.
Synovial telocytes are a distinct interstitial cell population lost in RA, and their depletion may impair lymphatic function and drive disease progression. While not yet actionable clinically, telocyte biology may emerge as a target for restoring tissue homeostasis in inflammatory arthritis.
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