MiRNA Overexpression Induces Cardiomyocyte Proliferation In Vivo

Abstract

Many millions of muscle cells in the heart are lost following a heart attack (myocardial infarction), and replacing or regenerating these cells is of fundamental importance for the long-term recovery of heart function. Therefore, any strategy that induces proliferation of adult cardiomyocytes in the region damaged by ischemic injury is of great interest in regenerative medicine. A major hurdle for replenishing damaged myocardium is that adult mammalian cardiomyocytes, unlike those of zebrafish, have a very limited proliferative capacity.1,2 Indeed, a recent landmark study showed that the mouse heart loses the capacity to regenerate sufficient cells to recover from a myocardial infarction just a few days after birth.3 It is therefore very important to understand why the hearts of zebrafish and those of very young mice can completely regenerate after an infarction whereas those of the adult human heart cannot and instead form a scar that leads to compromised myocardial function. In a recent issue of Nature,4 Eulalio and colleagues shed some light on this issue by identifying a number of microRNA (miRNA) species that have the capacity to induce cardiomyocyte cell proliferation and improve heart function following myocardial infarction in rodents.