To proliferate or not to proliferate

Abstract

This editorial refers to ‘Cardiomyocyte cell cycle control and growth estimation in vivo —an analysis based on cardiomyocyte nuclei’ by S. Walsh et al ., pp. 365–373, this issue. Cardiomyocytes in mammalian hearts undergo significant reduction in their cell proliferation capacity soon after birth, which is not disputed. However, it remains uncertain whether the adult heart contains a limited capacity for cell proliferation. Through the use of immunohistochemical staining methods, it has been reported that adult mouse cardiomyocytes can re-enter the cell cycle and duplicate.1,2 However, the origin of the cell-cycle-positive cells was not determined. Others reported permanent inhibition of cell-cycle progression in adult cardiomyocytes in mice.3 With advances in lineage tracing technology, a recent genetic labelling study demonstrated that stem or precursor cells did not contribute significantly to the formation of cardiomyocytes during normal ageing up to 1 year in the mouse. In contrast, precursor cells may participate in the formation of new cardiomyocytes after cardiac injury.4 In humans, high myocyte proliferation rates that could result in the exchange of all cardiomyocytes within 5 years have been reported by employing immunostaining technology on sections of human patients who died of acute myocardial infarction.5 In contrast, using 14C dating analyses in humans, Bergmann et al .6 reported that cardiomyocytes are renewed with a gradual decrease from …