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Mitochondrial impairment serves as a key driver of ferroptosis by elevating reactive oxygen species and promoting the iron-mediated Fenton process, wherein ferrous ions facilitate the transformation of hydrogen peroxide into highly reactive hydroxyl radicals, thereby exacerbating oxidative damage and triggering ferroptotic cell death (121, 125, 126)

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Real-life examples underscore this shift: many individuals are already considering generic options as part of their treatment plans

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