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Transient Ca 2+ influx facilitates OXPHOS and ATP production, whereas prolonged influx disturbs several dehydrogenases of the TCA cycle and ATP synthase and triggers increased opening of mitochondrial permeability transition pores (mPTPs), which damages OXPHOS to burst ROS and form a positive feedback loop between Ca 2+ and ROS, where ROS enhances Ca 2+ influx and vice versa, initiating glycolysis to activate the M1 phenotype [74, 75]

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