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Taking account of the mechanisms of ferroptosis, GSH-depleted methods have been extensively exploited for antitumor therapy based on GSH-enhanced GPX4 inactivity and LPO accumulation

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Tumor cells deficient in mitophagy exhibit heightened susceptibility to ferroptosis inducers due to the loss of this protective mechanism (46)

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The mechanisms controlling their transcription, post-transcriptional mRNA fate and post-translational modifications remain largely uncharacterized