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It plays critical roles in protecting the body from oxidative stress, maintaining cellular functions, and supporting healthy immune function.[1,4] Many factors can increase cellular exposure to oxidative insult, and therefore increase cellular consumption of nutrients-such as glutathione-that provide antioxidant activity

In OA models, ACSL4 inhibition dramatically decreases ferroptosis-associated lipid peroxidation ( 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

doi: 10.1016/S0006-3495(96)79317-7 Heuer, KH, Mackay, JP, Podzebenko, P, Bains, NPS, Weiss, AS, King, GF and EasterbrookSmith, SB (1996)

PloS One 9, e87251

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