{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T19:41:51Z","timestamp":1783712511693,"version":"3.55.0"},"reference-count":33,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2025,7,9]],"date-time":"2025-07-09T00:00:00Z","timestamp":1752019200000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003453","name":"Natural Science Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["2024A1515012811"],"award-info":[{"award-number":["2024A1515012811"]}],"id":[{"id":"10.13039\/501100003453","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Anim Models and Exp Med"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Osteoarthritis (OA) is a common degenerative joint disease characterized by the progressive degradation of articular cartilage. Mitochondrial dysfunction and autophagy, including mitophagy, have been implicated in OA pathogenesis. Long noncoding RNAs (lncRNA) are emerging as key regulators in various cellular processes, but their roles in OA, particularly in chondrocytes, remain poorly understood. This study explores the involvement of lncRNA\u2010GCH1 in regulating mitophagy and its impact on chondrocyte function and cartilage degradation in OA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Primary chondrocytes were isolated from the cartilage tissues of OA patients and healthy controls. lncRNA\u2010GCH1 expression was assessed using RNA\u2010seq, reverse transcription quantitative polymerase chain reaction, and RNA fluorescence in\u00a0situ hybridization. Functional assays, including Cell Counting Kit\u20108 (CCK\u20108), colony formation, flow cytometry, and Western blotting, were used to evaluate the effects of lncRNA\u2010GCH1 knockdown on chondrocyte proliferation, apoptosis, cell cycle, and mitophagy. Mitochondrial function was assessed by measuring adenosine triphosphate production, reactive oxygen species levels, and mitochondrial membrane potential. In\u00a0vivo, a murine OA model was used to examine the impact of lncRNA\u2010GCH1 knockdown on cartilage degradation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>lncRNA\u2010GCH1 was upregulated in OA chondrocytes and localized in the cytoplasm. Knockdown of lncRNA\u2010GCH1 enhanced cell proliferation and arrested cell cycle in G0\/G1. It also suppressed mitophagy, improved mitochondrial function, and reduced matrix\u2010degrading enzyme expression\u2014effects that were reversed by rapamycin treatment. Meanwhile, lncRNA\u2010GCH1 knockdown reduced PTEN\u2010induced kinase 1 (PINK1) aggregation and in\u00a0vivo local inhibition of PINK1 diminished cartilage degradation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>lncRNA\u2010GCH1 regulates mitophagy in OA chondrocytes, influencing mitochondrial function and matrix degradation. Targeting lncRNA\u2010GCH1 may offer a potential therapeutic approach for OA treatment.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ame2.70057","type":"journal-article","created":{"date-parts":[[2025,7,10]],"date-time":"2025-07-10T03:05:32Z","timestamp":1752116732000},"page":"1253-1267","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Long noncoding <scp>RNA<\/scp><scp>GCH1<\/scp> mediates mitophagy via the <scp>PTEN<\/scp>\u2010induced kinase 1\/Parkin pathway to drive chondrocyte dysfunction and cartilage degeneration in osteoarthritis"],"prefix":"10.1002","volume":"8","author":[{"given":"Gang","family":"Zeng","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery, Sun Yat\u2010sen Memorial Hospital Sun Yat\u2010sen University  Guangzhou PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yujun","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of 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