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The mitochondrial damage in CI/RI results in a burst of ROS and calcium overload synergized with pro-apoptotic Bax causing the mitochondrial membrane permeability transition pore to open, followed by the release of Cyt C and activation of caspase-9 as described in 2.3 above, which in turn activates caspase-3, ultimately leading to apoptotic cell death (Xu et al., 2021a) (Figure 1)

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