Document Detail

Signaling pathways in cardiac myocyte hypertrophy.
MedLine Citation:
PMID:  9405163     Owner:  NLM     Status:  MEDLINE    
When a heart responds to increased workload it does so by hypertrophy. This is characterized by an increase in cell size in the absence of cell division, and is accompanied by distinct qualitative and quantitative changes in gene expression. The use of cardiomyocytes in cell culture has identified, besides mechanical loading, a range of substances, such as cytokines, growth factors, catecholamines, vasoactive peptides and hormones, involved in mediating cardiac myocyte hypertrophy, and has enabled the molecular dissection of the pathways involved in signal transduction. Many different pathways are activated in response to different hypertrophic stimuli, and a growing number of crosslinks are being characterized between these pathways. Recent evidence suggests a central role for Ras in transmitting signals from G-protein coupled receptors, from growth factor receptors and from cytokine receptors not only down the Raf-MEK-ERK pathway to the nucleus, but also to various other cytosolic effectors. The evaluation of distinct morphological phenotypes, together with biochemical data on gene regulation, suggests that interactions between different signaling pathways take place. Each stimulus provokes a typical cellular phenotype and different stimuli may act alone or in concert in a synergistic, antagonistic or permissive manner. Consequently, hypertrophy of cultured cardiomyocytes cannot simply be characterized as the reversal to the fetal gene expression program. Thus, hypertrophic growth of the heart may similarly be the result of a complex combinatorial action of various stimuli, which may also lead to different morphological and biochemical phenotypes with distinct physiological properties.
M A Hefti; B A Harder; H M Eppenberger; M C Schaub
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  29     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1997 Nov 
Date Detail:
Created Date:  1998-02-23     Completed Date:  1998-02-23     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2873-92     Citation Subset:  IM; S    
Copyright Information:
Copyright 1997 Academic Press Limited.
Institute of Pharmacology, University of Zurich, Zurich, CH-8057, Switzerland.
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MeSH Terms
Calcium-Calmodulin-Dependent Protein Kinases / physiology
Cardiomegaly / pathology,  physiopathology*
Cells, Cultured
GTP-Binding Proteins / physiology
Growth Substances / physiology
Signal Transduction / physiology*
Stress, Mechanical
ras Proteins / physiology
Reg. No./Substance:
0/Growth Substances; EC Protein Kinases; EC 3.6.1.-/GTP-Binding Proteins; EC Proteins

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

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