Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 34, Issue 2, Pages 91-105Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1006/jmcc.2001.1506
Keywords
myocyte division; Ki67; apoptosis; necrosis; myocyte size and number
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Funding
- NHLBI NIH HHS [HL-65557, HL-65573, HL-39902, HL-38132] Funding Source: Medline
- NIA NIH HHS [AG-15756, AG-17042] Funding Source: Medline
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Introduced several decades ago, the dogma persists that ventricular myocytes are terminally differentiated cells and cardiac repair by myocyte regeneration is completely inhibited shortly after birth. On the basis that cardiac myocytes are unable to divide in the adult heart, myocyte growth under physiologic and pathologic conditions is believed to be restricted to cellular hypertrophy. Evidence is presented to indicate that this old paradigm has to be changed to include myocyte replication as a significant component of the cellular processes of ventricular remodeling, Importantly, myocyte death, apoptotic and necrotic in nature, has to be regarded as an additional critical variable of the multifactorial events implicated in the alterations of cardiac anatomy and myocardial structure of the decompensated heart. Methodologies are currently available to recognize and measure quantitatively the contribution of myocyte size, number and death to the adaptation of the overloaded heart and its progression to cardiac failure. (C) 2002 Elsevier Science Ltd.
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