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demonstrated that activation of the nuclear receptor FXR by BAs significantly suppresses ferroptosis by upregulating multiple ferroptosis gatekeepers, including GPX4, FSP1, PPAR, SCD1 and ACSL3 (67)

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

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)

Notably, MUC1 is overexpressed in a variety of adenocarcinomas, including breast, ovary, colon, rectum and prostate[13-15]