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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

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No mutagenic or genotoxic effects have been reported

This metabolic reprogramming creates an addiction to intracellular and extracellular nutrients (i.e., strong dependencies on nutrients), which may result in acquired resistance to cell death [13]