In the present study, we found that (1) telmisartan improved cardiac remodeling in patients with diabetes; (2) the development of cardiac fibrosis in the diabetic rat was markedly decreased after telmisartan treatment through the PPARδ pathway; (3) the regulatory mechanism of PPARδ on the hyperglycemia-induced fibrosis was dependent on the activation of STAT3. Here, STAT3 is linked to diabetes mellitus.