### Transient Regenerative Potential of the Neonatal Mouse Heart Porello et al Science . 2011;331:1078–1080 The regenerative capacity of adult human hearts after infarction seems vestigial at best, perhaps because of the poor proliferative capacity of terminally differentiated cardiomyocytes and desecration of the local environment that would otherwise be conducive of stem cell-mediated repair or loss of stem cells, or both. In a recent edition of the journal Science , Porello et al set a new benchmark in this field by showing that the hearts of neonatal mice have, in contrast, an impressive regenerative capacity after surgical resection, albeit one that is lost almost immediately as cardiomyocytes exit the cell cycle and mature. In a technical tour de force, Porello et al1 report that day 1 neonatal mice subjected to resection of the apex of the left ventricle (amounting to ∼15% of the ventricular myocardium) not only survive but also show complete regeneration of the myocardium and restoration of cardiac function. Furthermore, they provide evidence that the predominant mechanism involved is not differentiation of stem cells, but transient dedifferentiation and proliferation of cardiomyocytes in both the border and remote zones of the heart. In contrast, resection of a lesser amount of apical myocardium in day 7 neonates, at a time after terminal differentiation of cardiomyocytes has already taken place, resulted in markedly increased mortality and failure of myocardial regeneration, with wound repair by scar formation only. It has long been known that in adult mammals, the heart is one of the least regenerative organs in the body. As a result, repair after massive tissue injury, as occurs with myocardial infarction, is limited to replacement of the myocardium by dense collagenous scar tissue. This impairs contractile function, resulting in adverse remodelling and, in severe cases, ventricular dilation, heart failure, and death. To explore if intracardiac …