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Autocrine IGF1 signaling mediates pancreatic tumor cell dormancy in the absence of oncogenic drivers

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)

It helps protect cells from oxidative damage and supports mitochondrial function, allowing cells to perform at their best

Therefore, novel drug delivery systems to combat oxidative stress in COPD are needed