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Chondrocytes were treated with 10\u2009ng\/mL interleukin\u20101\u03b2 (IL\u20101\u03b2) or 5\u2009\u03bcM Erastin (ferroptosis inducer). IL\u20101\u03b2 or Erastin treatment inhibited cell viability and glutathione levels; increased Fe<jats:sup>2+<\/jats:sup>, lipid reactive oxygen species and malondialdehyde production; and decreased glutathione peroxidase 4, ferritin light chain and solute carrier family 7 member 11 levels. The overexpression of METTL3 facilitated the N6\u2010methyladenosine methylation of high mobility group box 1 (HMGB1). HMGB1 overexpression reversed the effect of sh\u2010METTL3 on IL\u20101\u03b2\u2010treated chondrocytes. A KOA rat model was established by the injection of monosodium iodoacetate into the joints and successful model establishment was confirmed by haematoxylin and eosin staining and Safranin O\/Fast Green staining. METTL3 depletion alleviated cartilage damage, the inflammatory response, ferroptosis and knee pain in KOA model rats, and these effects were reversed by the addition of HMGB1. In conclusion, METTL3 depletion inhibited ferroptosis and the inflammatory response, and ameliorated cartilage damage and knee pain during KOA progression by regulating HMGB1.<\/jats:p>","DOI":"10.1002\/cbin.12229","type":"journal-article","created":{"date-parts":[[2024,8,12]],"date-time":"2024-08-12T05:13:55Z","timestamp":1723439635000},"page":"1755-1765","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["METTL3 mediated ferroptosis in chondrocytes and promoted pain in KOA via HMGB1 m6A modification"],"prefix":"10.1002","volume":"48","author":[{"given":"Tianchi","family":"Bao","sequence":"first","affiliation":[{"name":"Department of Orthopedics and Traumatology Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine Suzhou 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