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Article

Disinhibition of SOD-2 expression to compensate for a genetically determined NO deficit in endothelial cells--brief report.

Arteriosclerosis, thrombosis, and vascular biology - 1 Nov 2009

Asif Abdul R, Hecker Markus, Cattaruzza Marco

Abstract excerpt

OBJECTIVE: Homozygosity for the -786C-variant of the human nos-3 gene is a risk factor for coronary artery disease (CAD). Interestingly, affected individuals develop CAD more frequently but not earlier than the general population. METHODS AND RESULTS: Genotyped primary human umbilical vein endothelial cells (ECs) were exposed to fluid shear stress (FSS) and analyzed for nitric oxide (NO) and superoxide anion...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 19696404
DOI: 10.1161/ATVBAHA.109.190678

Genes

CAD

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