During post-natal maturation of the mammalian heart, proliferation of cardiomyocytes
essentially ceases as cardiomyocytes withdraw from the cell cycle and develop blocks at the
G0/G1 and G2/M transition phases of the cell cycle. As a result, the response of the
myocardium to acute stress is limited to various forms of cardiomyocyte injury, which can be
modified by preconditioning and reperfusion, whereas the response to chronic stress is
dominated by cardiomyocyte hypertrophy and myocardial remodeling. Acute myocardial …