Source:http://linkedlifedata.com/resource/pubmed/id/15781121
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2005-3-22
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pubmed:abstractText |
The multifunctional Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases. This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0163-7258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
106
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
39-55
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:15781121-Animals,
pubmed-meshheading:15781121-Arrhythmias, Cardiac,
pubmed-meshheading:15781121-Calcium-Calmodulin-Dependent Protein Kinase Type 2,
pubmed-meshheading:15781121-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:15781121-Cardiomyopathies,
pubmed-meshheading:15781121-Humans,
pubmed-meshheading:15781121-Myocardium,
pubmed-meshheading:15781121-Signal Transduction
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pubmed:year |
2005
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pubmed:articleTitle |
Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmias.
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pubmed:affiliation |
Vanderbilt University Medical Center, 383 Preston Research Building, Nashville, TN 37232-6300, USA. mark.anderson@vanderbilt.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, N.I.H., Extramural
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