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.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 在美国，继发于2型糖尿病（DM）的心肌病和心力衰竭正在成为一个巨大的健康问题，患者人群稳步增加。 我们的研究小组和其他人收集的证据表明，高血糖症和相关的代谢异常直接影响心肌细胞的收缩力和能量利用，我们假设由过度蛋白糖基化诱导的线粒体形态和生化缺陷起着重要作用。 本项目旨在利用啮齿动物糖尿病模型和先进的显微技术，确定长期高血糖引起的线粒体解剖和功能变化。