我们前期的研究表明，急性心肌缺血再灌注（MIR）后跨室壁Cx43表达的不均一增加是MIR易发心律失常的重要原因，但是糖尿病性心肌病（DCM）是否也存在跨室壁复极离散以及中层心肌细胞Cx43在其中所起的作用并不清楚。另外，以往认为PPAR-γ激动剂罗格列酮具有良好的降低血糖、抑制心律失常的作用，但是近来的研究又表明它降低心肌Cx43表达而抑制心肌细胞离子通道活性。因此我们设计该课题，比较DCM左心室三层心肌细胞单相动作电位和离子通道的改变以及跨室壁缝隙连接蛋白分布的异质性，探讨DCM发生MVA的蛋白基础和电生理机制；同时观察罗格列酮和其他PPAR-γ激动剂、拮抗剂对这些变化的直接影响，明确PPAR-γ在DCM发生MVA中所起的作用与机制。以上研究可以探讨糖尿病患者使用PPAR-γ激活剂的安全性，为DCM患者MVA 的治疗寻找新的药物靶点，对改善这些病人的预后提供科学依据。

Our previous study showed that transmural heterogeneity of Cx43 expression in acute myocardial ischemia reperfusion (MIR) increased, which is the important reason for the malignant ventricular arrhythmia(MVA). Whether there is transmural heterogeneity of Cx43 in diabetic cardiomyopathy (DCM) and their physiological mechanisms are unclear. Although it was showed that the PPAR-γ agonist rosiglitazone could lower blood sugar and improve arrhythmia, recently research has found that it could decrease myocardial Cx43 expression and change the ion channel activity of myocardial cells. Therefore, we design the project to compare monophasic action potentials and ionic channels among three myocardial layers and explore the physiological mechanisms of MVA in DCM. We will also observe respective direct effects of rosiglitazone and other PPAR-γ agonists and antagonists on these changes and further explore the roles and mechanisms of PPAR-γ for MVA in the DCM. All above researchs can be looking for new drug targets for MVA with DCM and discussing PPAR-γ activator's security on diabets, which have important reference values in improving the prognosis of patients with DCM.