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Similarly, it has also been shown that GPX4 is degraded by interacting with different autophagic receptors after Fin56 (type 3 ferroptosis inducer) or excessive copper treatment, triggering ferroptosis [205, 206]

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On the other hand, this drug enhances RT-induced ferroptosis, leading to mitochondrial stress and ROS accumulation, which further induces the release of mtDNA