Cardiac Repair after Myocardial Infarction

A glycoprotein secreted by epicardial cells has a salutary effect on cardiomyocytes and cardiac repair after myocardial infarction in animal models. Heart failure, a leading cause of death in industrialized nations, is caused by damage to or loss of contracting cardiac muscle cells known as cardiomyocytes. Wei and colleagues 1 recently described a strategy to restore these cells. They reported that increasing the levels of follistatin-like 1 (FSTL1) derived from the epicardium, which are depleted after myocardial infarction, promotes myocardial repair and regeneration by stimulating the proliferative capacity of existing cardiomyocytes (Figure 1). Normally, cardiomyocytes in adult mammals proliferate at an extremely low rate (approximately 1% of cardiomyocytes per year undergo cell division). During ischemic injury — for example, a myocardial infarction . . .