Genetic insights into cardiovascular function and diseas

我们实验室感兴趣的一个发展中领域是研究线粒体调节的新机制，这可能对心血管功能很重要。我们最近发现，肿瘤抑制基因p53深刻地影响小鼠的运动能力，我们已经确定了作为细胞色素c氧化酶复合物的组装因子的介质基因。这一发现可能为我们以前观察到的化疗药物引起的p53依赖性氧化剂生成和心力衰竭提供了分子解释。我们现在正在开展研究，将这些基本观察结果中的一些转化为人类研究。 我们的实验室也在分子解剖容易接近的对动脉粥样硬化重要的人类细胞，以获得对疾病过程的新见解。使用无偏的方法，我们已经确定单核细胞和巨噬细胞转录因子作为反应性疾病标志物和疾病介质。正在进行研究，以阐明候选基因的分子机制，在发病机制，使用小鼠和人类模型系统。

A developing area of interest to our laboratory is investigating novel mechanisms of mitochondrial regulation that may be important for cardiovascular function. We have recently shown that the tumor suppressor gene p53 profoundly affects exercise capacity in mice, and we have identified the mediator gene as an assembly factor of the cytochrome c oxidase complex. This finding may offer a molecular explanation for some of our previous observations of p53 dependent oxidant generation and heart failure by chemotherapeutic agents. We are now initiating studies to translate some of these basic observations to human studies. Our laboratory is also molecularly dissecting easily accessible human cells important for atherosclerosis to gain new insights into the disease process. Using unbiased approaches, we have identified monocyte and macrophage transcription factors as a reactive disease markers and mediators of disease. Studies are underway to elucidate the molecular mechanisms of candidate genes in pathogenesis using mouse and human model systems.