Mitochondrial Metabolism and Endothelial Dysfunction

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