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rdf:type |
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|
lifeskim:mentions |
umls-concept:C0001645,
umls-concept:C0006675,
umls-concept:C0018801,
umls-concept:C0027061,
umls-concept:C0030685,
umls-concept:C0086418,
umls-concept:C0332161,
umls-concept:C0391871,
umls-concept:C0439799,
umls-concept:C0542341,
umls-concept:C0597198,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1963578
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pubmed:issue |
19
|
|
pubmed:dateCreated |
2003-5-20
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|
pubmed:abstractText |
Chronic beta-adrenergic receptor (beta-AR) blockade improves cardiac contractility and prolongs survival in patients with heart failure; however, the mechanisms underlying these favorable responses are poorly understood. Stress-induced activation of the sympathetic nervous system results in protein kinase A (PKA)-mediated phosphorylation of the calcium (Ca2+) release channel/cardiac ryanodine receptor (RyR2), required for cardiac excitation-contraction (EC) coupling, activating the RyR2 channel, and increasing cardiac contractility. The hyperadrenergic state of heart failure results in leaky RyR2 channels attributable to PKA hyperphosphorylation and depletion of the stabilizing FK506 binding protein, FKBP12.6. We tested the hypothesis that improved cardiac muscle function attributable to beta-AR blockade is associated with restoration of normal RyR2 channel function in patients with heart failure.
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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 |
|
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pubmed:status |
MEDLINE
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pubmed:month |
May
|
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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 |
20
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pubmed:volume |
107
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2459-66
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:12743001-Adrenergic beta-Antagonists,
pubmed-meshheading:12743001-Blood Pressure,
pubmed-meshheading:12743001-Calcium Channels,
pubmed-meshheading:12743001-Cardiac Volume,
pubmed-meshheading:12743001-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:12743001-Diastole,
pubmed-meshheading:12743001-Female,
pubmed-meshheading:12743001-Heart,
pubmed-meshheading:12743001-Heart Failure,
pubmed-meshheading:12743001-Heart Transplantation,
pubmed-meshheading:12743001-Humans,
pubmed-meshheading:12743001-Macromolecular Substances,
pubmed-meshheading:12743001-Male,
pubmed-meshheading:12743001-Middle Aged,
pubmed-meshheading:12743001-Perfusion,
pubmed-meshheading:12743001-Phosphorylation,
pubmed-meshheading:12743001-Receptors, Adrenergic, beta,
pubmed-meshheading:12743001-Ryanodine Receptor Calcium Release Channel,
pubmed-meshheading:12743001-Tacrolimus Binding Proteins
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pubmed:year |
2003
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pubmed:articleTitle |
Beta-blockers restore calcium release channel function and improve cardiac muscle performance in human heart failure.
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pubmed:affiliation |
Center for Molecular Cardiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|
