Renin-angiotensin system (RAS) is activated in diabetes. The rise of angiotension II (Ang II) stimulates the cardiac fibroblast proliferation and the alteration of collagen metabolism through AT1 receptor on cell surface, causing the myocardium interstitial and perivascular fibrosis, and the ventricular myocardium rigidity and diastolic function disturbance, leading to the clinical symptoms of diabetic cardiomyopathy (DCM). The main members of RAS including Ang II, Ang-(1-7), Ac-SDKP and ATR play the important role in the development of DCM. This article reviewed the interactions between RAS and endothelin (ET), reactive oxygen species (ROS), transforming growth factor-beta 1 (TGF-beta 1), nuclear factor-kappa b (NF-kappaB), signal transduction system and apoptosis in DCM.