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0 reviewsObesity-related osteoarthritis (OA) and the molecular mechanisms governingmultiple joint structural changes that occur with obesity are not well understood. This study investigated the progression of obesity in mice and validatedthe results using human joint samples post-arthroplasty. The results show thatobesity is associated with the degeneration of the cartilage layer and abnormalremodeling of the subchondral bone layer, and this occurs alongside aging andDNA damage in chondrocytes, osteoclasts, and stem cells. Regulation of p53-FOXO3 gene loop expression in response to DNA damage effectively inhibitschondrocyte apoptosis, catabolism, and excessive osteoclast differentiation,while the intra-articular delivery of a lentivirus expressing FOXO3 to mousejoints alleviates the progression of OA. The excessive differentiation of subchondral bone marrow osteoclasts is ferroptosis-dependent and driven by thesenescence-associated secretory phenotype. The results have identified multiple potential targets for future research into the progression of obesityrelated OA.
