BECN1 and myocardial infarction: Considering the prominent effects of intramyocardial MSCs transplantation on scar fibrosis, echocardiographic, cardiomyocyte contractile and intracellular Ca2+ as well as mitochondrial properties, and the fact that such effects were ablated by Beclin1 haploinsufficiency, it is likely that MSCs therapy improve post-MI injury through inhibition of apoptosis /inflammation in an autophagy-dependent manner, other than the rare cell regenerative ability in post-infarct hearts.