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Modulation of the Cardiomyocyte Cell Cycle in Genetically Altered Animals



    Corresponding author
    1. Herman B Wells Center and Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
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Address for correspondence: Prof. Loren J. Field, Ph.D., Wells Center for Pediatric Research, Indiana University School of Medicine, 702 Barnhill Drive, Rm. 2666, Indianapolis, IN 46202. Fax: 317-274-537.


Abstract: Many forms of cardiovascular disease are associated with cardiomyocyte loss via apoptosis and/or necrosis. Although there is currently debate regarding the level at which adult cardiomyocytes can reenter the cell cycle and proliferate, it is clear that the intrinsic regenerative growth capacity is insufficient to reverse the progression to failure in badly injured hearts. The ability to reactivate cardiomyocyte proliferation in damaged hearts might permit regenerative growth, provided that the nascent cells are able to participate in a functional syncytium with the surviving myocardium. In this review, techniques commonly used to monitor cardiomyocyte cell cycle activity in normal and injured hearts are discussed. In addition, several genetic models are described wherein the expression of fundamental cell cycle regulatory proteins has been altered in cardiomyocytes.