MECHANISM OF DIABETIC CARDIOMYOPATHY

糖尿病心肌病的机制

• 批准号: 8361919
• 负责人: Wolfgang H Dillmann
• 金额: $ 2.47万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-04-01 至 2012-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361919
• 关键词: Affect; Biochemical; Cardiac Myocytes; Cardiomyopathies; Defect; Funding; Grant; Health; Heart failure; Hyperglycemia; Image Analysis; Metabolic; Microscopic; Mitochondria; National Center for Research Resources; Play; Principal Investigator; Protein Glycosylation; Research; Research Infrastructure; Resources; Rodent Model; Role; Secondary to; Source; Technology; United States National Institutes of Health; cost; 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. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Cardiomyopathy and heart failure secondary to type 2 diabetic mellitus (DM) is becoming an enormous health 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.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 随着患者人数的稳步增加，2 型糖尿病 (DM) 继发的心肌病和心力衰竭正在成为美国的一个巨大的健康问题。 我们的团队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性和能量使用，我们假设过度蛋白质糖基化引起的线粒体形态和生化缺陷起着重要作用。 该项目旨在利用糖尿病啮齿动物模型和先进的显微技术来确定长期高血糖引起的线粒体解剖和功能变化。