MST1 and myocardial infarction: However, suppression of endogenous Mst1 with cardiac-specific overexpression of a dominant-negative form of Mst1 (Mst1K59R) inhibited cardiomyocytes apoptosis, reduced the extent of myocardial damage and improved cardiac function after I/R injury or myocardial infarction (Yamamoto et al., 2003; Odashima et al., 2007).