糖尿病心肌病（DCM）指无高血压、冠心病等传统心衰危险因素的糖尿病患者出现的心功能受损，是2型糖尿病（T2DM）促进心衰发生的重要原因，近年来得到广泛关注。冠脉微血管病变是DCM的重要病理特征及潜在机制。T2DM是冠脉微血管病变的重要因素，但机制尚不明确。T2DM患者除了糖脂代谢紊乱外，还存在严重的支链氨基酸（BCAA）代谢障碍，而BCAA代谢紊乱与冠脉微血管损伤及DCM的关系尚无探讨。课题组预实验首次发现BCAA代谢障碍可抑制基质相互作用分子1（STIM1）的表达，引起小鼠冠脉内皮细胞损伤。因此，在前期研究基础上，本课题将充分论证BCAA代谢障碍在T2DM冠脉微血管损伤和DCM中发挥的作用并探索其潜机制，为DCM的发病及进展提出新的解释，为降低T2DM心衰风险提供新的理论依据。

Diabetic cardiomyopathy (DCM), defined as the presence of myocardial dysfunction in the absence of conventional risk factor, such as hypertension, coronary artery disease, significantly contribute to heart failure associated with T2DM. The coronary microvascular abnormalities and thereby reduction in myocardial blood flow reserve induced by T2DM are potential contributors to DCM. However, the mechanism underling coronary microvascular abnormalities in T2DM was not fully understood. Branched-chain amino acids (BCAA) catabolic defect was established in strong relationship with variable pathogenesis in T2DM in our previous research, but if it was involved in coronary microvascular abnormalities and DCM was still unknown. The results of preliminary experiment manifested that catabolic defect of BCAA reduced expression of STIM1 and related to dysfunction and apoptosis of mouse coronary endothelial cells (MCECs). Based on this information, we hypothesized that BCAA catabolic defect may promote coronary microvascular abnormalities therefore contribute to DCM. In this study, we will verify the hypophyses systematically, thus provide new explanation and therapeutic strategy to DCM and T2DM associated heart failure.