MECHANISM OF DIABETIC CARDIOMYOPATHY

糖尿病心肌病的机制

• 批准号: 8169620
• 负责人: Wolfgang H Dillmann
• 金额: $ 1.19万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169620
• 关键词: Affect; Biochemical; Cardiac Myocytes; Cardiomyopathies; Computer Retrieval of Information on Scientific Projects Database; Defect; Funding; Grant; Heart failure; Hyperglycemia; Institution; Metabolic; Microscopic; Mitochondria; Play; Protein Glycosylation; Research; Research Personnel; Resources; Rodent Model; Role; Secondary to; Source; Technology; United States National Institutes of Health; diabetic; diabetic cardiomyopathy; patient population

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Cardiomyopathy and heart failure secondary to type 2 diabetic mellitus (DM) is becoming an enormous hearth issue in the US with a steady increase in patient population. Evidence collected by our groups and others now indicates that hyperglycemia and associated metabolic abnormalities directly affect the contractility and the energy usage of cardiomyocytes and we hypothesize morphological and biochemical defects of mitochondria induced by excessive protein glycosylation plays a major role. This project aims to determine anatomical and functional changes in mitochondria caused by prolonged hyperglycemia using rodent models of DM and advanced microscopic technologies.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 继发于2型糖尿病性梅洛蒂斯（DM）继发的心肌病和心力衰竭正在成为美国的一个巨大壁炉问题，患者人群稳定增加。 我们的小组和其他人收集的证据现在表明，高血糖和相关的代谢异常直接影响心肌细胞的收缩力和能量使用，我们假设由过度蛋白质糖基化诱导的线粒体的形态和生化缺陷在主要角色上起着主要作用。 该项目旨在确定使用DM和晚期显微镜技术的啮齿动物模型长期高血糖引起的线粒体的解剖和功能变化。