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rdf:type |
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lifeskim:mentions |
umls-concept:C0006675,
umls-concept:C0018801,
umls-concept:C0033095,
umls-concept:C0205421,
umls-concept:C0225828,
umls-concept:C0669368,
umls-concept:C0871261,
umls-concept:C1514559,
umls-concept:C1704632,
umls-concept:C1705165,
umls-concept:C1706817,
umls-concept:C2700061,
umls-concept:C2911692
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pubmed:issue |
25
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pubmed:dateCreated |
2008-6-24
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pubmed:abstractText |
Defects in cardiomyocyte Ca(2+) cycling are a signature feature of heart failure (HF) that occurs in response to sustained hemodynamic overload, and they largely account for contractile dysfunction. Neuronal nitric oxide synthase (NOS1) influences myocyte excitation-contraction coupling through modulation of Ca(2+) cycling, but the potential relevance of this in HF is unknown.
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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 |
|
|
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1524-4539
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pubmed:author |
pubmed-author:BénitahJean-PierreJP,
pubmed-author:BIOZZISS,
pubmed-author:CharueDominiqueD,
pubmed-author:Fernandez-VelascoMariaM,
pubmed-author:GómezAna MariaAM,
pubmed-author:HeymesChristopheC,
pubmed-author:JaisserFrédéricF,
pubmed-author:LoyerXavierX,
pubmed-author:MartyIsabelleI,
pubmed-author:MayerBerndB,
pubmed-author:MercadierJean-JacquesJJ,
pubmed-author:MilliezPaulP,
pubmed-author:RichardSylvainS,
pubmed-author:RobidelEstelleE,
pubmed-author:Sainte-MarieYannisY,
pubmed-author:SamuelJane-LiseJL,
pubmed-author:VangheluwePeterP,
pubmed-author:VaudinEmilieE,
pubmed-author:VinetLaurentL,
pubmed-author:ZhangWeiW
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pubmed:issnType |
Electronic
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pubmed:day |
24
|
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pubmed:volume |
117
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
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pubmed:pagination |
3187-98
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pubmed:meshHeading |
pubmed-meshheading:18541744-Animals,
pubmed-meshheading:18541744-Aorta,
pubmed-meshheading:18541744-Blood Pressure,
pubmed-meshheading:18541744-Calcium,
pubmed-meshheading:18541744-Cell Separation,
pubmed-meshheading:18541744-Disease Models, Animal,
pubmed-meshheading:18541744-Disease Progression,
pubmed-meshheading:18541744-Enzyme Activation,
pubmed-meshheading:18541744-Heart Failure,
pubmed-meshheading:18541744-Humans,
pubmed-meshheading:18541744-Mice,
pubmed-meshheading:18541744-Mice, Transgenic,
pubmed-meshheading:18541744-Myocardial Contraction,
pubmed-meshheading:18541744-Myocytes, Cardiac,
pubmed-meshheading:18541744-Nitric Oxide Synthase Type I,
pubmed-meshheading:18541744-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18541744-Signal Transduction,
pubmed-meshheading:18541744-Ventricular Function, Left
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pubmed:year |
2008
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pubmed:articleTitle |
Cardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling.
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pubmed:affiliation |
Institut National de Santé et de Recherché Médicale (INSERM), Unit 689, Centre de Recherché Cardiovasculaire Lariboisière, Paris, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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