| pubmed-article:10966823 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10966823 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:10966823 | lifeskim:mentions | umls-concept:C0000768 | lld:lifeskim |
| pubmed-article:10966823 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:10966823 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:10966823 | pubmed:dateCreated | 2000-10-30 | lld:pubmed |
| pubmed-article:10966823 | pubmed:abstractText | Progressive deterioration of cardiac contractility is a central feature of congestive heart failure (CHF) in humans. In this report we review those studies that have addressed the idea that alterations of intracellular calcium (Ca(2+)) regulation is primarily responsible for the depressed contractility of the failing heart. The review points out that Ca(2+)transients and contraction are similar in non-failing and failing myocytes at very slow frequencies of stimulation (and other low stress environments). Faster pacing rates, high Ca(2+)and beta-adrenergic stimulation reveal large reductions in contractile reserve in failing myocytes. The underlying cellular basis of these defects is then considered. Studies showing changes in the abundance of L-type Ca(2+)channels, Ca(2+)transport proteins [sarcoplasmic reticulum Ca(2+)ATPase (SERCA2), phospholamban (PLB), Na(+)/Ca(2+) exchanger (NCX)] and Ca(2+) release channels (RYR) in excitation-contraction coupling and Ca(2+)release and uptake by the sarcoplasmic reticulum (SR) are reviewed. These observations support our hypotheses that (i) defective Ca(2+)regulation involves multiple molecules and processes, not one molecule, (ii) the initiation and progression of CHF inolves defective Ca(2+)regulation, and (iii) prevention or correction of Ca(2+)regulatory defects in the early stages of cardiac diseases can delay or prevent the onset of CHF. | lld:pubmed |
| pubmed-article:10966823 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10966823 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10966823 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10966823 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10966823 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10966823 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:10966823 | pubmed:issn | 0022-2828 | lld:pubmed |
| pubmed-article:10966823 | pubmed:author | pubmed-author:HouserS RSR | lld:pubmed |
| pubmed-article:10966823 | pubmed:author | pubmed-author:WeisserJJ | lld:pubmed |
| pubmed-article:10966823 | pubmed:author | pubmed-author:PiacentinoVV3... | lld:pubmed |
| pubmed-article:10966823 | pubmed:copyrightInfo | Copyright 2000 Academic Press. | lld:pubmed |
| pubmed-article:10966823 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10966823 | pubmed:volume | 32 | lld:pubmed |
| pubmed-article:10966823 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10966823 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10966823 | pubmed:pagination | 1595-607 | lld:pubmed |
| pubmed-article:10966823 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
| pubmed-article:10966823 | pubmed:meshHeading | pubmed-meshheading:10966823... | lld:pubmed |
| pubmed-article:10966823 | pubmed:meshHeading | pubmed-meshheading:10966823... | lld:pubmed |
| pubmed-article:10966823 | pubmed:meshHeading | pubmed-meshheading:10966823... | lld:pubmed |
| pubmed-article:10966823 | pubmed:meshHeading | pubmed-meshheading:10966823... | lld:pubmed |
| pubmed-article:10966823 | pubmed:meshHeading | pubmed-meshheading:10966823... | lld:pubmed |
| pubmed-article:10966823 | pubmed:meshHeading | pubmed-meshheading:10966823... | lld:pubmed |
| pubmed-article:10966823 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10966823 | pubmed:articleTitle | Abnormalities of calcium cycling in the hypertrophied and failing heart. | lld:pubmed |
| pubmed-article:10966823 | pubmed:affiliation | Cardiovascular Research Group, Molecular and Cellular Cardiology Laboratories, Department of Physiology, 3400 North Broad Street, Philadelphia, PA 19140, USA. srhouser@unix.temple.edu | lld:pubmed |
| pubmed-article:10966823 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10966823 | pubmed:publicationType | Review | lld:pubmed |
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