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For acute myocardial infarction, H 2 gas could activate mK ATP and regulate mitochondrial membrane potential to equilibrize the level of myocardial NAD+ (the precursor of ATP synthesis) and the production of mitochondrial ATP, thus alleviating myocardial I/R injury (Yoshida et al., 2012)

ER stresstriggered by CS in COPDescalates lipid peroxidation, activating ferroptosis pathways (61, 62)

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