SUV39H1 and myocardial infarction: To understand the underlying mechanism, primary rat neonatal ventricular myocytes were exposed to ischemic or oxidative stress, leading to upregulation of the histone H3K9 methyltransferase SUV39H and downregulation of SIRT1. In addition, inhibition of SUV39H activity by chaetocin in wild-type mice and SUV39H-knockout mice protected against induced MI.