Diabetes alters function of several growth factors, including fibroblast growth factor (FGF), by altering their expression or by glycosylation.Although, FGF supplementation prevents cardiac ischemia/reperfusion injury, it has significant mitotic activity, a potential obstacle for clinical application.As mitotic domains of aFGF is separate from its biological active domains, we developed a novel mutant from recombinant human acidic FGF (MaFGF), by deleting the nuclear translocation domain (N-terminal 26 amino acids).Ma FGF has no mitotic activity and shows protective action against oxidative stress.As target tissue damage in diabetes, is largely mediated through oxidative stress we investigated protective effects of MaFGF on diabetic cardiomyopathy, both in vivo and in vitro.