<scp>CCT7</scp> Regulates <scp>TRAF6</scp> ‐Mediated Autophagy to Promote Posttraumatic Joint Contracture

Posttraumatic joint contracture (PTJC) is a prevalent complication of joint injury, characterised by marked reductions in both active and passive joint motion. Previous studies have indicated that the chaperonin-containing T-complex 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-β1. Knockdown of CCT7 markedly reduced the expression of α-SMA and COL-I and suppressed fibroblast migration, while simultaneously promoting autophagy, as indicated by increased LC3-II and Beclin-1 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 vivo experiments demonstrated that CCT7 knockdown improved joint range of motion, reduced the expression of fibrosis-related proteins, enhanced autophagy and ultimately alleviated fibrosis.