Survey of studies examining mammalian cardiomyocyte DNA synthesis.

Increases in cardiac mass during fetal life arise predominantly as a consequence of cardiomyocyte proliferation. During neonatal life, there is a transition from hyperplastic to hypertrophic growth such that further increases in myocardial mass are typically not accompanied by cardiomyocyte proliferation. In the adult myocardium, it is generally believed that the vast majority of cardiomyocytes do not proliferate. This view is supported in part by clinical observations: functionally significant myocardial regeneration has not been documented in diseases and/or injuries that result in cardiomyocyte loss. Furthermore, primary myocardial tumors are rarely observed in adults. Although these findings suggest that the proliferative capacity of adult cardiomyocytes is quite low, they do not exclude the existence of a limited degree of hyperplastic growth in either the normal or diseased myocardium. Toward this end, a number of studies examining the proliferative capacity of cardiomyocytes in experimental animals have been reported. Because genome reduplication is a prerequisite for cell proliferation, the majority of these studies have used various methodologies to monitor cardiomyocyte DNA synthesis as a first approximation of cell division. In the present survey, issues that we consider pertinent for accurate assessment of cardiomyocyte DNA synthesis are discussed. The literature examining cardiomyocyte DNA synthesis during normal and pathological myocardial growth is then summarized.