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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2002-1-4
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pubmed:abstractText |
A long-standing hypothesis has been that hypertrophy is compensatory and by normalizing wall stress acts to maintain normal cardiac function. Epidemiological data, however, have shown that cardiac hypertrophy is associated with increased mortality, thus casting doubt on the validity of this hypothesis.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Dopamine beta-Hydroxylase,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/Heterotrimeric GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Protein v-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta,
http://linkedlifedata.com/resource/pubmed/chemical/Retroviridae Proteins, Oncogenic,
http://linkedlifedata.com/resource/pubmed/chemical/beta-Adrenergic Receptor Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1524-4539
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
105
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
85-92
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11772881-Adenylate Cyclase,
pubmed-meshheading:11772881-Animals,
pubmed-meshheading:11772881-Cardiomegaly,
pubmed-meshheading:11772881-Constriction,
pubmed-meshheading:11772881-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:11772881-Dopamine beta-Hydroxylase,
pubmed-meshheading:11772881-Echocardiography,
pubmed-meshheading:11772881-GTP-Binding Protein alpha Subunits, Gq-G11,
pubmed-meshheading:11772881-Heart,
pubmed-meshheading:11772881-Heterotrimeric GTP-Binding Proteins,
pubmed-meshheading:11772881-Mice,
pubmed-meshheading:11772881-Mice, Knockout,
pubmed-meshheading:11772881-Mice, Transgenic,
pubmed-meshheading:11772881-Mitogen-Activated Protein Kinases,
pubmed-meshheading:11772881-Myocardium,
pubmed-meshheading:11772881-Oncogene Protein v-akt,
pubmed-meshheading:11772881-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:11772881-Receptors, Adrenergic, beta,
pubmed-meshheading:11772881-Retroviridae Proteins, Oncogenic,
pubmed-meshheading:11772881-Signal Transduction,
pubmed-meshheading:11772881-beta-Adrenergic Receptor Kinases
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pubmed:year |
2002
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pubmed:articleTitle |
Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress.
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pubmed:affiliation |
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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