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Although prior work indicates that ferroptosis acts as a central hub linking reactive oxygen species to autophagy and apoptosis, this study does not establish its priority within the cascade of oxidative stress, neuroinflammation, and multimodal cell death, particularly regarding microglial ferroptosis and its contribution to secondary neuronal injury

Because GSH is a cofactor for GST isoforms, disruptions in GSH synthesis have the potential to severely disturb the detoxifying capacity of hepatic GSTs (Hardwick et al

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Class III FINs such as FIN56 act by indirect inhibiting and inactivating GPX4 via the squalene synthase-mevalonate pathway, which participates in the mitochondrial electron transport chain and also functions as endogenous lipophilic antioxidants [40, 108]