Document Detail


Myocyte proliferation in the developing heart.
MedLine Citation:
PMID:  21538685     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Regulation of organ growth is critical during embryogenesis. At the cellular level, mechanisms controlling the size of individual embryonic organs include cell proliferation, differentiation, migration, and attrition through cell death. All these mechanisms play a role in cardiac morphogenesis, but experimental studies have shown that the major determinant of cardiac size during prenatal development is myocyte proliferation. As this proliferative capacity becomes severely restricted after birth, the number of cell divisions that occur during embryogenesis limits the growth potential of the postnatal heart. We summarize here current knowledge concerning regional control of myocyte proliferation as related to cardiac morphogenesis and dysmorphogenesis. There are significant spatial and temporal differences in rates of cell division, peaking during the preseptation period and then gradually decreasing toward birth. Analysis of regional rates of proliferation helps to explain the mechanics of ventricular septation, chamber morphogenesis, and the development of the cardiac conduction system. Proliferation rates are influenced by hemodynamic loading, and transduced by autocrine and paracrine signaling by means of growth factors. Understanding the biological response of the developing heart to such factors and physical forces will further our progress in engineering artificial myocardial tissues for heart repair and designing optimal treatment strategies for congenital heart disease.
Authors:
David Sedmera; Robert P Thompson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2011-05-02
Journal Detail:
Title:  Developmental dynamics : an official publication of the American Association of Anatomists     Volume:  240     ISSN:  1097-0177     ISO Abbreviation:  Dev. Dyn.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-11     Completed Date:  2011-10-03     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  9201927     Medline TA:  Dev Dyn     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1322-34     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Wiley-Liss, Inc.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation / genetics
Cell Proliferation*
Gene Expression Regulation, Developmental
Heart / embryology*,  growth & development
Humans
Models, Biological
Morphogenesis / genetics,  physiology
Myocardium / metabolism
Myocytes, Cardiac / metabolism,  physiology*
Grant Support
ID/Acronym/Agency:
HL50582/HL/NHLBI NIH HHS; HL91452/HL/NHLBI NIH HHS; P20 RR016434/RR/NCRR NIH HHS; P20 RR016434-09S1/RR/NCRR NIH HHS; R01 HL033756/HL/NHLBI NIH HHS; R01 HL050582/HL/NHLBI NIH HHS; R01 HL050582-13/HL/NHLBI NIH HHS; R21 HL091452/HL/NHLBI NIH HHS; R21 HL091452-02/HL/NHLBI NIH HHS; RR16434/RR/NCRR NIH HHS
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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