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3.11 Neuroprotective efficacy of GO@GSH-FA on neuronal injury post-ischemia-reperfusion To elucidate the neuroprotective potential of GO@GSH-FA, we performed both histological and molecular analyses on cerebral ischemia-reperfusion injury lesions

for example, research has uncovered augmented ferroptosis due to the up-regulation of autophagy genes (103) and has demonstrated that nuclear receptor co-activator 4 (NCOA4)-induced ferritin-mediated phagocytosis, RAB7A-dependent lipid phagocytosis, BECN1-induced systemic inhibition, STAT3-promoted lysosomal membrane permeability, and HSP90-related molecular chaperone-mediated autophagy may all lead to ferroptosis

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As a result, several contradictory findings have been reported (Prinz et al., 2011