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In OA cartilage tissues and IL-1β–stimulated chondrocyte models, iron accumulation, elevated levels of lipid peroxidation byproducts such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), and downregulation of the antioxidant enzyme GPX4 have been widely reported ( Ferroptosis-related alterations are not limited to cartilage