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doi: 10.3389/fphar.2022.899198
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However, this preservation of mitochondrial function creates a paradox: by maintaining the electron transport chain, CHAC1 inadvertently supplies the ROS that propagate iron-dependent lipid peroxidation ( via two convergent mechanisms: the direct depletion of glutathione and the indirect facilitation of mitochondrial ROS production, thereby coupling sustained metabolic activity to ferroptotic cell death under cysteine limitation
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