SOD1 and myocardial infarction: In vitro: Inhibits mitochondrial permeability transition pore (mPTP) opening, reduces ROS generation, enhances SOD activity, improves cell viability post-H/R injury; In vivo: Reduces myocardial infarction area, alleviates myocardial injury; Improves mitochondrial morphology, inhibits apoptosis, targets ischemic myocardium mitochondria