| Literature DB >> 21239247 |
Abstract
Division and proliferation of the terminally differentiated ventricular heart muscle cell in the adult mammal is not activated after injury such as that caused by a myocardial infarction. We do not understand how mitosis is irreversibly blocked in these myocytes during early development. Mammalian cardiac muscle, unlike skeletal muscle, cannot regenerate. Knowledge of the mechanisms that control the cardiac myocyte cell cycle would allow us to design reagents or procedures to initiate repair or regeneration of the adult myocardium following injury. Ideally, we would like to be able to revert cardiac muscle cells in intact heart muscle to the biochemical state they were in during early fetal growth when they were actively dividing and proliferating. This article briefly reviews what is currently known about the mechanism which so tightly suppresses the mitotic activity of these highly differentiated cells.Entities:
Year: 1992 PMID: 21239247 DOI: 10.1016/1050-1738(92)90030-V
Source DB: PubMed Journal: Trends Cardiovasc Med ISSN: 1050-1738 Impact factor: 6.677