Mitochondrial Metabolism and Endothelial Dysfunction

$532,923P01FY2008HLNIH

Boston University Medical Campus, Boston MA

Investigators

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Abstract

This proposal will test the hypothesis that mitochondrial damage is increased in those individuals at greater[unreadable] risk for coronary atherosclerotic disease (CAD), or those currently diagnosed with CAD, compared with age[unreadable] matched non-CAD individuals. Mitochondrial DNA (mtDNA) damage will be assessed as an indicator of[unreadable] mitochondrial damage in leukocytes. MtDNA damage will be determined using quantitative PCR (QPCR), a[unreadable] highly sensitive technique that quantifies DNA damage. For these studies, mtDNA damage will be[unreadable] quantified from leukocytes from CAD patients and non-CAD controls. The overall aim of these studies is to[unreadable] determine whether mitochondrial damage and dysfunction contribute to impaired production and bioactivity[unreadable] of endothelium-derived nitric oxide in atherosclerosis.

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