| pubmed-article:16616906 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16616906 | lifeskim:mentions | umls-concept:C0026844 | lld:lifeskim |
| pubmed-article:16616906 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
| pubmed-article:16616906 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:16616906 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:16616906 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:16616906 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:16616906 | pubmed:dateCreated | 2006-6-26 | lld:pubmed |
| pubmed-article:16616906 | pubmed:abstractText | Reactive oxygen species (ROS) have been shown to function as important signaling molecules in the cardiovascular system. Vascular smooth muscle cells (VSMCs) contain several sources of ROS, among which the NADPH oxidases are predominant. In VSMCs, ROS mediate many pathophysiological processes, such as growth, migration, apoptosis and secretion of inflammatory cytokines, as well as physiological processes, such as differentiation, by direct and indirect effects at multiple signaling levels. Therefore, it becomes critical to understand the different roles ROS play in the physiology and pathophysiology of VSMCs. | lld:pubmed |
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