FOCAL POINT  Cardiomyocytes from neonatal mice are able to proliferate and replace damaged heart tissue, but they lose this regenerative capacity a week after birth. Ignacio Flores (left), Esther Aix (right), and colleagues reveal that this is partially due to a rapid shortening of cardiomyocyte telomeres that causes cell cycle arrest and binucleation. Telomerase-deficient mice undergo premature telomere shortening, and are therefore unable to regenerate damaged heart tissue even at one-day old, resulting in larger fibrotic regions (blue) 28 days after injury. The proliferative and regenerative capacity of these cardiomyocytes is restored by knocking out p21, a cell cycle inhibitor that is activated by telomere shortening.

PHOTO COURTESY OF THE AUTHORS