MECHANISM OF DIABETIC CARDIOMYOPATHY

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 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心脏问题，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DM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。

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.