| pubmed-article:18068669 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18068669 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:18068669 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:18068669 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:18068669 | lifeskim:mentions | umls-concept:C0036226 | lld:lifeskim |
| pubmed-article:18068669 | lifeskim:mentions | umls-concept:C0001476 | lld:lifeskim |
| pubmed-article:18068669 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
| pubmed-article:18068669 | lifeskim:mentions | umls-concept:C2347946 | lld:lifeskim |
| pubmed-article:18068669 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18068669 | pubmed:dateCreated | 2008-3-21 | lld:pubmed |
| pubmed-article:18068669 | pubmed:abstractText | The Ca(2+) ATPase of sarcoplasmic reticulum has a prominent role in excitation/contraction coupling of cardiac muscle, as it induces relaxation by sequestering Ca(2+) from the cytoplasm. The stored Ca(2+) is in turn released to trigger contraction. We review here experiments demonstrating that in cardiac myocytes Ca(2+) signaling and contractile activation are strongly altered by pharmacological inhibition or transcriptional down-regulation of SERCA. On the other hand, kinetics, and intensity of Ca(2+) signaling are improved by SERCA overexpression following delivery of exogenous cDNA by adenovirus vectors. Experiments on adrenergic hypertrophy demonstrate SERCA down-regulation, consistent with its pathogenetic involvement in cardiac hypertrophy and failure, as also shown in other experimental models and clinical studies. Compensation by alternate Ca(2+) signaling proteins, including functional activation and increased expression of Na(+)/Ca(2+) exchanger and TRPC proteins has been observed. These compensatory mechanisms, including calcineurin activation, remain to be clarified and are a most important subject of current studies. | lld:pubmed |
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| pubmed-article:18068669 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18068669 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18068669 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18068669 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18068669 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18068669 | pubmed:issn | 1090-2104 | lld:pubmed |
| pubmed-article:18068669 | pubmed:author | pubmed-author:InesiGiuseppe... | lld:pubmed |
| pubmed-article:18068669 | pubmed:author | pubmed-author:PrasadAnand... | lld:pubmed |
| pubmed-article:18068669 | pubmed:author | pubmed-author:RajendraPilan... | lld:pubmed |
| pubmed-article:18068669 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18068669 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:18068669 | pubmed:volume | 369 | lld:pubmed |
| pubmed-article:18068669 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18068669 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18068669 | pubmed:pagination | 182-7 | lld:pubmed |
| pubmed-article:18068669 | pubmed:dateRevised | 2011-5-17 | lld:pubmed |
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| pubmed-article:18068669 | pubmed:meshHeading | pubmed-meshheading:18068669... | lld:pubmed |
| pubmed-article:18068669 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18068669 | pubmed:articleTitle | The Ca2+ ATPase of cardiac sarcoplasmic reticulum: Physiological role and relevance to diseases. | lld:pubmed |
| pubmed-article:18068669 | pubmed:affiliation | California Pacific Medical Center Research Institute, 475 Brannan Street, San Francisco, CA 94107, USA. | lld:pubmed |
| pubmed-article:18068669 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18068669 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:18068669 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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