Moreover, deletion of the p16ink4+ gene in cardiomyocytes significantly improved cardiac function and reduced cardiac scar size and SASP after myocardial infarction in a mouse model [53], demonstrating a role of senescent cardiomyocytes in contributing to pathological cardiac remodeling and heart dysfunction following myocardial infarction. This evidence concerns the gene CDKN2A and myocardial infarction.