MicroRNA-93 elevation after myocardial infarction is cardiac protective

Abstract

Coronary Artery Disease (CAD) is one of the most serious diseases that endangers human health worldwide, myocardial infarction (MI) is an acute form of CAD. Recent developments in MI therapies have resulted in significant reductions in mortality. However, subsequent chronic congestive heart failure and ventricle remodeling plagues an increasing number of MI patients. MicroRNAs (miR) have been reported to be involved in the process of cardiac remodeling, a recent study shows that miR-93 is elevated in the blood of CAD patients. Similar to human CAD, we found miR-93 is elevated both in ventricle tissue and blood in mice MI model, and miR-93 is secreted from cardiomyocytes cultured under hypoxia. Interestingly, miR-93 inhibits apoptosis and protects cardiomyocytes from ischemia/reperfusion injury. In other type of ischemic disease like stoke and peripheral arterial disease, miR-93 shows long term protective effects via enhancing angiogenesis, inducing macrophage M2 polarization and antioxidant effects. These effects are favorable for ventricle remodeling inhibition after MI. In a pilot experiment, we indicated that miR-93 knockdown deteriorate cardiac remodeling in 30days after MI in mice models. Therefore, we hypothesize that miR-93 upregulation and secretion from cardiomyocytes after MI is adaptive, which could inhibit cardiac remodeling and heart failure.