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The susceptibility of cancer cells to ferroptotic death is determined by the antagonism between the cellular metabolic activities that trigger lipid oxidation and the cellular antioxidant systems that counteract it [34]
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The primers used are listed in the Supplementary Table 2
Combined interventions targeting MPC dysfunction, ROS buffering systems such as the Nrf2GSH axis, or mitophagy pathways including PINK1, may disrupt the self-sustaining signalmetabolism circuit and offer a strategy to delay or reverse acquired therapeutic resistance
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