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Similarly, we found that DDX5 was downregulated in injured condylar cartilage of patients as well as the condyles of UAC\u2010induced TMJOA mice. The chondrocyte\u2010specific deletion of\n                      <jats:italic>Ddx5<\/jats:italic>\n                      aggravated tissue destruction in TMJOA modeling by inducing degradation of extracellular matrix (ECM).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The loss of DDX5 facilitated chondrocyte degradation and the occurrence of joint inflammation in condylar chondrocytes. In addition, the local injection of AAV overexpressing DDX5 significantly alleviated inflammation, cartilage degradation, and subchondral bone loss in TMJOA mice. RNA\u2010seq analysis revealed that the DDX5 deficiency mostly activated the TNF\u2010induced nuclear factor\u2010kappa B (NF\u2010\u03baB) signaling pathway causing the occurrence of TMJOA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Mechanistically, the inhibition of DDX5 accelerated cartilage degeneration by activating TNF\u2010induced NF\u2010\u03baB signaling. Thus, DDX5 emerges as a potential effective drug target for future therapeutic approaches in TMJOA.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/odi.15294","type":"journal-article","created":{"date-parts":[[2025,3,8]],"date-time":"2025-03-08T03:33:39Z","timestamp":1741404819000},"page":"2229-2242","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["<scp>DDX5<\/scp>\n                    Alleviates Temporomandibular Joint Osteoarthritis via\n                    <scp>TNF<\/scp>\n                    \u2010Induced\n                    <scp>NF<\/scp>\n                    \u2010\n                    <scp>\u03baB<\/scp>\n                    Signaling Pathway"],"prefix":"10.1111","volume":"31","author":[{"given":"Qingqing","family":"Liang","sequence":"first","affiliation":[{"name":"Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Research Institute of Stomatology Nanjing University  Nanjing 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