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In PC12 cells, exposure to dopamine resulted in a marked disruption of mitochondrial bioenergetic functions, leading to an approximately 40% decrease in cell viability, along with signs of apoptotic nuclear alterations and heightened activities of caspase 3 and caspase 9

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While Nrf2 signaling is often suppressed globally in COPD lungs, its dysfunction in macrophages may paradoxically promote ferritinophagy-mediated iron retention through nuclear receptor coactivator 4 (NCOA4), overwhelming ferroprotein (FPN)-mediated iron export and unintentionally fueling ferroptosis

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