Mitochondrial Metabolism and Endothelial Dysfunction

这项提议将检验这样一个假设，即线粒体损伤在那些个体中增加， 与年龄相比，冠状动脉粥样硬化性疾病（CAD）的风险，或目前诊断为CAD的患者 匹配的非CAD个体。线粒体DNA（mtDNA）损伤将被评估为 白细胞线粒体损伤。将使用定量PCR（QPCR）， 高灵敏度的技术来量化DNA损伤。在这些研究中，mtDNA损伤将是 从CAD患者和非CAD对照的白细胞定量。这些研究的总体目标是 确定线粒体损伤和功能障碍是否导致生产和生物活性受损 内皮源性一氧化氮在动脉粥样硬化中的作用。

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.