Linked Life Data

9405163

Source:http://linkedlifedata.com/resource/pubmed/id/9405163

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1998-2-23
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-2828
pubmed:author
pubmed:copyrightInfo
Copyright 1997 Academic Press Limited.
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2873-92
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Signaling pathways in cardiac myocyte hypertrophy.
pubmed:affiliation
Institute of Pharmacology, University of Zurich, Zurich, CH-8057, Switzerland.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't