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Exosomes are involved in facilitating calcification, and their biogenesis may be linked to autophagy disruption. However, whether autophagy disruption regulates exosome\u2010mediated calcification in OA remains to be elucidated. Here, B\u2010cell receptor\u2010associated protein 31 (BAP31) was identified as a key mechanosensitive regulator bridging this gap. Mechanical stimulation activated BAP31 in chondrocytes. Protein docking, coimmunoprecipitation assays, and competitive pull\u2010down assays demonstrated that activated BAP31 competes with autophagy\u2010related 14 (ATG14) for binding to syntaxin 17 (STX17), thereby disrupting the STX17\u2013ATG14 complex, which is essential for autophagosome\u2012lysosome fusion. This disruption led to the accumulation of autophagosomes, which in turn drove the release of exosomes that facilitated pathological cartilage calcification. Critically, intra\u2010articular delivery of adeno\u2010associated virus\u2010mediated BAP31 shRNA restored autophagosome\u2012lysosome fusion, suppressed exosome release, and attenuated cartilage calcification and degeneration in a rat OA model. Collectively, these findings identify BAP31 as a mechanical stress\u2010responsive switch that couples impaired autophagy to exosome\u2010mediated calcification, highlighting its potential as a therapeutic target for OA.<\/jats:p>","DOI":"10.1002\/advs.202520140","type":"journal-article","created":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T07:35:58Z","timestamp":1787988958000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["BAP31 Drives Cartilage Calcification through Disruption of Autophagosome\u2013Lysosome Fusion in Osteoarthritis"],"prefix":"10.1002","author":[{"given":"Zhi\u2010hua","family":"Xu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Oral &amp; Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology The Fourth Military Medical University  Xi'an China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruo\u2010xin","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Oral &amp; Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Orthodontics, School of Stomatology The Fourth Military Medical University Xi'an China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"He","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Oral &amp; Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral and Maxillofacial Surgery, School of Stomatology The Fourth Military Medical University  Xi'an Shaanxi 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