〔Abstract〕 Objective To explore the effect ofadeno-associated virussense transfection up-regulating the expression level of the growth and differential factor 11(GDF11)in vivoon aortic injury in type 2 diabetic mellitus rats(T2DM). Methods Nine-week-old male SD rats were randomly selected to establish a T2DM model by using high-sugar and high-fat chow plus small-dose streptozotocin(STZ) combined induction. Both normal rats and diabetic model rats were randomly divided into five groups: blank control group(Control group), negative virus control group(NC group), GDF11adeno-associated virusgroup(GDF11 group), diabetic group(DM group), and diabetic + GDF11adeno-associated virusgroup(DM+GDF11 group). After 8 weeks of feeding, the serum concentrations of insulin(INS), advanced glycosylation end products(AGES), recombinant growth transforming factor 11(GDF11), total cholesterol(T-CHO), triglycerides(TG), low-density lipoproteins(LDL-C), high-density lipoproteins(HDL-C), asymmetric dimethylarginine(ADMA), and malondialdehyde(MDA) were assayed in the rats; periodic acid-schiff stain(PAS stain) was used to observe the sites of glycogen deposition, and hematoxylin-eosin staining(HE) was used to observe vascular damage. Scanning electron microscopy was used to observe the damage of vascular endothelial cells and vascular elastic fibers, and protein blotting and immunohistochemistry were used to detect the expression levels of vascular injury-related proteins. Protein blotting and immunohistochemistry were used to detect the expression levels of vascular injury-related proteins. Results The biochemical indexes showed that the serum concentrations of AGES, T-CHO, TG, LDL-C and MDA were higher in the DM group than those in the Control group(P<0.05), the concentrations of INS, GDF11, HDL-C and ADMA were significantly lower than those in the Control group(P<0.05), and the concentrations of AGES and HDL-C were not significantly lower in the DM+GDF11 group compared with the DM group(P<0.05). HDL-C was not significantly different from the DM group, and several other data were improved(P<0.05). Pathological staining suggested that PAS staining in the DM group suggested that glycogen particles deposited in the endothelium and subendothelium of the aorta, HE staining observed thickening of the aortic mesentery, endothelial cells and elastic fibers broke off in an irregular alignment, and electron microscopy observed endothelial damage in the vasculature and elastic fibers broke off in the DM group, and these changes attenuated in the DM+GDF11 group. Protein blotting and immunohistochemistry indicated that the expression of endothelial cell-associated proteins decreased in the DM group(P<0.05), and mesenchymal markers elevated in the DM group(P<0.05), these proteins were regressed in the DM+GDF11 group, and the difference was statistically significant(P<0.05). Conclusion Increasing the expression level of GDF11in vivocan improve aortic vascular injury caused by diabetes mellitus, which is inferred that it may be related to the inhibition of endothelial mesenchymal transition to protect the function of vascular endothelial cells and thus improve vascular injury.