ArticleZhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery2026
[Protective effect and mechanism of TSPAN9-mediated mitocytosis in interleukin-1β-induced rat chondrocyte senescence].
Article in Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To investigate the regulatory role and molecular mechanisms of TSPAN9-mediated mitocytosis in an interleukin-1β (IL-1β)-induced rat chondrocyte senescence model, and to identify novel therapeutic targets for osteoarthritis (OA). Methods: Primary knee articular chondrocytes were isolated from the cartilage of knee joints harvested from 1-week-old male Sprague-Dawley rats and maintained in culture. Cell viability was assessed using the cell counting kit 8 (CCK-8) assay, and cell-cycle distribution was analyzed by flow cytometry to determine the optimal concentration and exposure time of IL-1β for model induction, thereby establishing an Results: Using CCK-8 assays and cell-cycle analysis, the staged rat chondrocyte senescence model induced by IL-1β (5 ng/mL), and defined 12, 24, and 48 hours as the E-OA, M-OA, and L-OA senescence phenotypes were successfully established, respectively. Model validation demonstrated that, with prolonged induction, the proportion of SA-β-gal-positive cells increased markedly, mitochondrial membrane potential progressively declined ( Conclusion: Impaired mitocytosis is an important pathological mechanism underlying IL-1β-induced chondrocyte senescence, and TSPAN9 overexpression may delay chondrocyte senescence by promoting mitocytosis in concert with KIF5B, thereby facilitating the clearance of damaged mitochondria and restoring intracellular homeostasis.
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