Aggravating: Increases cardiomyocyte apoptosis and oxidative stress by targeting KLF1 [257], enhances cardiac fibrosis after MI partially through targeting RASA1 [258], inhibits the angiogenesis of coronary microvascular endothelial cells in the ischemic heart [259]; Attenuating: Protects in vitro cells from hypoxia-induced apoptosis and excessive autophagy via the AKT/mTOR pathway by targeting PARP-1 [260], inhibits I/R-induced cardiac necroptosis at multiple layers [261]. This evidence concerns the gene PARP1 and myocardial infarction.