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Metformin, via the AMPK/ACC pathway, reshapes lipid utilization and reduces ACSL4 and 4-HNE positivity, thereby improving chondrocyte resistance to ferroptosis ( in vitro models, inhibiting cartilage chondroptosis and improving OA ( Excessive lipid metabolic reprogramming in OA significantly raises ferroptosis risk, so targeting lipid synthesis, transport, and degradation represents a promising upstream approach to reducing ferroptotic damage