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Description
This potential link between impaired mitochondrial bioenergetics and ferroptotic vulnerability may not be apparent in short-term in vitro experiments, which are typically conducted in nutrient-rich media that support metabolic flexibility and compensate for transient energy deficits, explaining why iron chelators only suppress ferroptosis in this context
Clark RA, Szot S, Williams MA, Kagan HM (1986) Oxidation of lysine side-chains of elastin by the myeloperoxidase system and by stimulated human neutrophils

(2008) Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression
This contributes to an escalating pandemic of cardiovascular disease, cancer, and respiratory disease [2, 3]