| pubmed-article:17876304 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17876304 | lifeskim:mentions | umls-concept:C0026844 | lld:lifeskim |
| pubmed-article:17876304 | lifeskim:mentions | umls-concept:C2610216 | lld:lifeskim |
| pubmed-article:17876304 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:17876304 | pubmed:dateCreated | 2008-3-3 | lld:pubmed |
| pubmed-article:17876304 | pubmed:abstractText | In non-excitable cells, activation of G-protein-coupled phospholipase C (PLC)-linked receptors causes the release of Ca(2+) from intracellular stores, which is followed by transmembrane Ca(2+) entry. This Ca(2+) entry underlies a small and sustained phase of the cellular [Ca(2+)](i) increases and is important for several cellular functions including gene expression, secretion and cell proliferation. This form of transmembrane Ca(2+) entry is supported by agonist-activated Ca(2+)-permeable ion channels that are activated by store depletion and is referred to as store-operated Ca(2+) entry (SOCE) and represents a major pathway for agonist-induced Ca(2+) entry. In excitable cells such as smooth muscle cells, Ca(2+) entry mechanisms responsible for sustained cellular activation are normally considered to be mediated via either voltage-operated or receptor-operated Ca(2+) channels. Although SOCE occurs following agonist activation of smooth muscle, this was thought to be more important in replenishing Ca(2+) stores rather than acting as a source of activator Ca(2+) for the contractile process. This review summarizes our current knowledge of SOCE as a regulator of vascular smooth muscle tone and discusses its possible role in the cardiovascular function and disease. We propose a possible hypothesis for its activation and suggest that SOCE may represent a novel target for pharmacological therapeutic intervention. | lld:pubmed |
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