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Excess Cu 2+ within cells can be transported to the mitochondria by ionophores, and FDX1 reduces Cu 2+ to Cu +

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TYRO3 induces anti-PD-1/PD-L1 therapy resistance by limiting innate immunity and tumoral ferroptosis

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High concentrations of tHA inhibited the expression of autophagy-related proteins beclin1 and LC3II in human PDLSCs (hPDLSCs), inducing excessive ROS production and leading to cell damage and apoptosis