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Chondrocyte ferroptosis facilitates the advancement of OA, as shown by both in vivo and in vitro studies [88]

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Its hallmark pathological features including cartilage degradation, subchondral bone sclerosis, osteophyte formation and synovial inflammation, are fueled by a complex interplay of inflammatory cascades, oxidative stress, and mechanical stress imbalance (57)

While individual results can vary, the data consistently shows positive trends