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It works as a "chain-breaking antioxidant" stopping free radical damage from cascading across membranes, like a firebreak preventing a blaze from spreading [3]

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Methods of Enzymology Vol

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Cabrera-Fuentes and Boisvert demonstrated that oscillatory cholesterol exposure uniquely accelerates atherosclerosis through IL-1-dependent neutrophil reprogramming, driving sustained macrophage dysfunction, autophagy impairment, and efferocytosis deficits ( - -GSH-GPX4 axis without recovery periods may deplete antioxidant reserves ( Cell type specific relevance in atherosclerosis Ferroptosis exhibits cell-type-specific impacts in the multi-cellular context of atherosclerosis