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Previous studies have indicated that the chaperonin\u2010containing T\u2010complex polypeptide (CCT) is involved in fibrotic processes. Thus, this study aims to explore the role of CCT7 in PTJC and clarify its underlying regulatory mechanisms. We found that CCT7 expression was significantly upregulated in PTJC joint tissues and in fibroblasts stimulated with TGF\u2010\u03b21. Knockdown of CCT7 markedly reduced the expression of \u03b1\u2010SMA and COL\u2010I and suppressed fibroblast migration, while simultaneously promoting autophagy, as indicated by increased LC3\u2010II and Beclin\u20101 levels and decreased p62 expression, thereby alleviating joint fibrosis. Interestingly, CCT7 interacted with TRAF6 to facilitate its ubiquitination and degradation. Knockdown of TRAF6 reversed the promoting effect of CCT7 knockdown on autophagy in fibroblasts and exacerbated fibrosis. Consistently, in\u00a0vivo experiments demonstrated that CCT7 knockdown improved joint range of motion, reduced the expression of fibrosis\u2010related proteins, enhanced autophagy and ultimately alleviated fibrosis.<\/jats:p>","DOI":"10.1111\/jcmm.71051","type":"journal-article","created":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T04:21:57Z","timestamp":1775622117000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>CCT7<\/scp>\n                    Regulates\n                    <scp>TRAF6<\/scp>\n                    \u2010Mediated Autophagy to Promote Posttraumatic Joint Contracture"],"prefix":"10.1111","volume":"30","author":[{"given":"Yutai","family":"Li","sequence":"first","affiliation":[{"name":"Department of Orthopaedics Huizhou Central People's Hospital  Huizhou China"},{"name":"Hui Zhou\u2010Hong Kong Bone Health Joint Research Center  Huizhou China"},{"name":"Huizhou Central People's Hospital 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