Abstract
Lower vertebrates such as newt and zebrafish are able to reactivate high levels of cardiomyocyte cell cycle activity in response to experimental injury resulting in apparent regeneration. In contrast, damaged myocardium is replaced by fibrotic scar tissue in higher vertebrates. This process compromises the contractile function of the surviving myocardium, ultimately leading to heart failure. Various strategies are being pursued to augment myocyte number in the diseased hearts. One approach entails the reactivation of cell cycle in surviving cardiomyocytes. Here, we provide a summary of methods to monitor cell cycle activity, and interventions demonstrating positive cell cycle effects in cardiomyocytes as well as discuss the potential utility of cell cycle regulation to augment myocyte number in diseased hearts.
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