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Circulation. 2006;113:1451-1463
doi: 10.1161/CIRCULATIONAHA.105.595181
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(Circulation. 2006;113:1451-1463.)
© 2006 American Heart Association, Inc.


Basic Science for Clinicians

Life and Death of Cardiac Stem Cells

A Paradigm Shift in Cardiac Biology

Piero Anversa, MD; Jan Kajstura, PhD; Annarosa Leri, MD; Roberto Bolli, MD

From the Cardiovascular Research Institute, Department of Medicine, New York Medical College, Valhalla, (P.A., J.K., A.L.); and the Institute of Molecular Cardiology, University of Louisville, Louisville, Ky (R.B.).

Correspondence to Piero Anversa, MD, Cardiovascular Research Institute, Vosburgh Pavilion, New York Medical College, Valhalla, NY 10595. E-mail piero_anversa@nymc.edu


Key Words: regeneration • heart failure • stem cells


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
The recognition that myocyte mitosis occurs in the fetal, neonatal, adult, and hypertrophied heart and that a pool of primitive, undifferentiated cells is present in the myocardium has put forward a different view of the biology of the heart. The new paradigm suggests that myocyte formation is preserved during postnatal life, in adulthood or senescence, pointing to a remarkable growth reserve of the heart throughout the course of life of the organism. This article reviews a large body of novel information, which has been obtained in the last 2 decades, in favor of the notion that the mammalian heart has the inherent ability to continuously replace its parenchymal cells and that this unexpected characteristic has important implications in understanding myocardial homeostasis, cardiac aging, and tissue repair.


*    The Heart Is a Self-Renewing Organ
 
The paradigm that the heart is a postmitotic organ incapable of regenerating parenchymal cells was established in the 1970s, and this dogma has profoundly conditioned basic and clinical research in cardiology for the last 3 decades. On the basis of this paradigm, cardiomyocytes undergo cellular hypertrophy1,2 but cannot be replaced either by entry into the cell cycle of a subpopulation of nonterminally differentiated myocytes or by activation of a pool of primitive cells that become committed to the myocyte lineage. The only response of cardiomyocytes to stress is hypertrophy and/or death. Therefore, a tremendous effort was made to identify the molecular mechanisms of myocyte hypertrophy and their genetic control. A sophisticated knowledge of various signaling pathways has been achieved, and our understanding of the . . . [Full Text of this Article]




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