1[1]Brownlee M.Biochemistry and molecular cell biology of diabetic complications[J].Nature,2001,414 (3):813-820.
2[2]Gareia Soriano F,Virng L,Jagtap P,et al.Diabetic endothelial dysfunction:the role of poly(ADP-ribose) polymerase activation[J].Nat Med,2001,7(1):108-113.
3[3]Pacher P,Liaudet L,Garda Soriano F,et al.Role of poly(ADP-ribose) polymerase activation in the development of myocardial and endothelial dysfunction in diabetes[J].Diabetes,2002,51(3):514-521.
5[5]Guzik TJ,Mussa S,Gastaldi D,et al.Mechanisms of increased vascular supemxide production in human diabetes mellitus:role of NAD (P) H oxidaseand endothelial nitric oxide synthase[J].Circulation,2002,105(7):1656-1662.
6[6]Zou MH,Shi C,Cohen RA.Oxidation of the zinc.thiolate complex and uncoupling of endothelial nitric oxide synthase by peroxynitrite[J].J Clin Invest,2002,109(3):817-826.
7[7]Chandra D,Ramana K V,Friedrich B,et al.Role of aldose reductase in TNF-alpha-induced apoptosis of vascular endothelial cells[J].Chem Biol Interact,2003,143 (3):605-612.
8[8]Abroad F K,He Z H,King G L.Molecular targets of diabetic cardiovascular complications[J].Current Drug Targets,2005,6 (4):487-494.
9[9]Caglayan E,Blaschke F,Takata Y,et al.Metabolic syndrome interdependence of the cardiovascular and metabolic pathways[J].Curr Opin Pharmacol,2005,5 (1):135-142.
10[10]Hansson L,Lindholm LH,Niskan en L,et al.Effect of angiotensin converting-enzyme inhibition compared with conventional therapy oncardiovascular morbidity and mortality in hypertension:the Captopril Prevention Project(CAPPP) randomised trial[J].Lancet,1999,353(2):611-616.