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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
13
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pubmed:dateCreated |
2006-9-26
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pubmed:abstractText |
Activation of cellular Ca2+ signaling molecules appears to be a fundamental step in the progression of cardiomyopathy and arrhythmias. Myocardial overexpression of the constitutively active Ca2+-dependent phosphatase calcineurin (CAN) causes severe cardiomyopathy marked by left ventricular (LV) dysfunction, arrhythmias, and increased mortality rate, but CAN antagonist drugs primarily reduce hypertrophy without improving LV function or risk of death.
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pubmed:grant |
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1524-4539
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pubmed:author |
pubmed-author:AndersonMark EME,
pubmed-author:BassMarthaM,
pubmed-author:ColbranRoger JRJ,
pubmed-author:GomezRey JRJ,
pubmed-author:GrueterChad ECE,
pubmed-author:GuanXiaoqunX,
pubmed-author:KannankerilPrinceP,
pubmed-author:KhooMichelle S CMS,
pubmed-author:LiJingdongJ,
pubmed-author:MaduErnest CEC,
pubmed-author:MendesLisaL,
pubmed-author:NiGeminG,
pubmed-author:OddisCarmine VCV,
pubmed-author:OlsonEric NEN,
pubmed-author:SinghMadhu VMV,
pubmed-author:WadzinskiBrian EBE,
pubmed-author:WuYuejinY,
pubmed-author:YangJinyingJ,
pubmed-author:YangYingboY,
pubmed-author:ZhangRongR
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pubmed:issnType |
Electronic
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pubmed:day |
26
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pubmed:volume |
114
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1352-9
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16982937-Amino Acid Sequence,
pubmed-meshheading:16982937-Animals,
pubmed-meshheading:16982937-Animals, Newborn,
pubmed-meshheading:16982937-Apoptosis,
pubmed-meshheading:16982937-Arrhythmias, Cardiac,
pubmed-meshheading:16982937-Benzylamines,
pubmed-meshheading:16982937-Calcineurin,
pubmed-meshheading:16982937-Calcium Signaling,
pubmed-meshheading:16982937-Calcium-Calmodulin-Dependent Protein Kinase Type 2,
pubmed-meshheading:16982937-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:16982937-Cells, Cultured,
pubmed-meshheading:16982937-Death, Sudden, Cardiac,
pubmed-meshheading:16982937-Disease Models, Animal,
pubmed-meshheading:16982937-Enzyme Induction,
pubmed-meshheading:16982937-Hypertrophy, Left Ventricular,
pubmed-meshheading:16982937-Isoproterenol,
pubmed-meshheading:16982937-Mice,
pubmed-meshheading:16982937-Mice, Transgenic,
pubmed-meshheading:16982937-Molecular Sequence Data,
pubmed-meshheading:16982937-Myocardial Contraction,
pubmed-meshheading:16982937-Myocytes, Cardiac,
pubmed-meshheading:16982937-Peptide Fragments,
pubmed-meshheading:16982937-RNA, Messenger,
pubmed-meshheading:16982937-Rats,
pubmed-meshheading:16982937-Sulfonamides,
pubmed-meshheading:16982937-Ventricular Dysfunction, Left
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pubmed:year |
2006
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pubmed:articleTitle |
Death, cardiac dysfunction, and arrhythmias are increased by calmodulin kinase II in calcineurin cardiomyopathy.
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pubmed:affiliation |
Department of Medicine, Vanderbilt University, Nashville, Tenn, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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