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rdf:type |
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lifeskim:mentions |
umls-concept:C0005486,
umls-concept:C0205245,
umls-concept:C0206588,
umls-concept:C0388148,
umls-concept:C0392673,
umls-concept:C0428876,
umls-concept:C1414463,
umls-concept:C1514873,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636
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pubmed:issue |
1
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pubmed:dateCreated |
2007-7-9
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pubmed:abstractText |
Downregulation and functional deactivation of the transcriptional coactivator PGC-1alpha has been implicated in heart failure pathogenesis. We hypothesized that the estrogen-related receptor alpha (ERRalpha), which recruits PGC-1alpha to metabolic target genes in heart, exerts protective effects in the context of stressors known to cause heart failure. ERRalpha(-/-) mice subjected to left ventricular (LV) pressure overload developed signatures of heart failure including chamber dilatation and reduced LV fractional shortening. (31)P-NMR studies revealed abnormal phosphocreatine depletion in ERRalpha(-/-) hearts subjected to hemodynamic stress, indicative of a defect in ATP reserve. Mitochondrial respiration studies demonstrated reduced maximal ATP synthesis rates in ERRalpha(-/-) hearts. Cardiac ERRalpha target genes involved in energy substrate oxidation, ATP synthesis, and phosphate transfer were downregulated in ERRalpha(-/-) mice at baseline or with pressure overload. These results demonstrate that the nuclear receptor ERRalpha is required for the adaptive bioenergetic response to hemodynamic stressors known to cause heart failure.
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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 |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1550-4131
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25-37
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pubmed:dateRevised |
2011-5-13
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pubmed:meshHeading |
pubmed-meshheading:17618854-Adaptation, Physiological,
pubmed-meshheading:17618854-Adenosine Triphosphate,
pubmed-meshheading:17618854-Animals,
pubmed-meshheading:17618854-Animals, Newborn,
pubmed-meshheading:17618854-Biological Markers,
pubmed-meshheading:17618854-Blood Pressure,
pubmed-meshheading:17618854-Cardiac Output, Low,
pubmed-meshheading:17618854-Cardiomegaly,
pubmed-meshheading:17618854-Energy Metabolism,
pubmed-meshheading:17618854-Female,
pubmed-meshheading:17618854-Gene Expression Profiling,
pubmed-meshheading:17618854-Heart,
pubmed-meshheading:17618854-Magnetic Resonance Spectroscopy,
pubmed-meshheading:17618854-Male,
pubmed-meshheading:17618854-Mice,
pubmed-meshheading:17618854-Mice, Inbred C57BL,
pubmed-meshheading:17618854-Mice, Knockout,
pubmed-meshheading:17618854-Muscle Contraction,
pubmed-meshheading:17618854-Myocytes, Cardiac,
pubmed-meshheading:17618854-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:17618854-RNA, Messenger,
pubmed-meshheading:17618854-Receptors, Estrogen,
pubmed-meshheading:17618854-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17618854-Transcription Factors,
pubmed-meshheading:17618854-Ventricular Pressure,
pubmed-meshheading:17618854-Ventricular Remodeling
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pubmed:year |
2007
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pubmed:articleTitle |
The nuclear receptor ERRalpha is required for the bioenergetic and functional adaptation to cardiac pressure overload.
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pubmed:affiliation |
Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, MO 63110, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural,
Research Support, N.I.H., Intramural
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