Endothelial nitric oxide synthase gene therapy for erectile dysfunction.
Basic science research on erectile physiology has been devoted to investigating the pathogenesis of erectile dysfunction (ED) and has led to the conclusion that ED is predominately a disease of vascular origin. It is well recognized that the incidence of ED dramatically increases in men who suffer from diabetes mellitus, hypercholesterolemia, and cardiovascular disease. Endothelial nitric oxide synthase (eNOS) is an important factor in cardiovascular homeostasis, angiogenesis, and erectile function. Given the impact of endothelial-derived nitric oxide (NO) in vascular biology, a great deal of research over the past decade has focused on the role of NO synthesis from the endothelium in normal erectile physiology as well as in disease states. Loss of the functional integrity of the endothelium and subsequent endothelial dysfunction plays an integral role in the occurrence of ED. Therefore, a likely target of gene therapy for the treatment of ED is eNOS. This communication reviews the role of eNOS in erectile physiology and discusses the alterations in eNOS expression in various vascular diseases of the penis. Putative gene therapy interventions to restore eNOS expression and subsequent endothelial function may represent an exciting new therapeutic strategy for the future treatment of ED.
Bivalacqua
Trinity J
TJ
Department of Urology, Tulane Health Sciences Center, 1430 Tulane Avenue SL42, New Orleans, LA 70112, USA.
Musicki
Biljana
B
Usta
Mustafa F
MF
Champion
Hunter C
HC
Kadowitz
Philip J
PJ
Burnett
Arthur L
AL
Hellstrom
Wayne J G
WJ
D007172:Erectile Dysfunction / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D015316:Genetic Therapy / Q000379:methods*; D006801:Humans; D008297:Male; D052250:Nitric Oxide Synthase Type III / Q000235:genetics* / Q000378:metabolism* / Q000627:therapeutic use
D052250:Nitric Oxide Synthase Type III