TP53 and myocardial infarction: This result has been supported by many studies, such as the study conducted by Kang et al., which demonstrated that activated ERK1/2 induced by H/R might be novel drug target in cardiomyocytes [30], and the studies of Tsoporis et al. and Liu et al., where they found that the activation of ERK1/2-p53 signaling pathway caused cardiomyocyte apoptosis after myocardial infarction or administration of anticancer drug doxorubicin [31, 32].