Are adult cardiocytes still able to proliferate?

In all mammals including humans, adult cardiocytes become post mitotic cells, while cardiac non muscle cells still have the capacity to proliferate, and cardiac hypertrophy in adults is known to be due to cardiocyte hypertrophy and non muscle cell hyperplasia. Such a dogma was supported by several, rather ancient, observations, and has been recently challenged by two different groups. Several new paradigms in cell biology have modified these views: the entire determinants of the cell cycle are now entirely known; apoptosis, and cardiac apoptosis, is central in the process of cell division, and has a rather complicated significance; telomeres are specialized DNA-protein structures that prevent end-to-end chromosome fusion, and are rather characteristic of germ and stem cells, these structures are maintained by telomerase. Using several markers, including telomerase activity, endogenous self-renewing, clonogenic and multipotent stem cells were identified in the adult myocardium in human, mice and rat. These cells are activated during cardiac overload or ischemia to produce new cardiocytes. New endothelial cells also appeared, and are likely to have a circulatory origin. The physiological importance of these new cells is debatable at the moment. Nevertheless, these findings provide an important new basis for cell cardiomyoplasty. It is also possible to envisage stimulation of the production and activity of these new cells to compensate for the lack of substance after myocardial infarction.