Pathophysiology of Erectile Dysfunction

被引：68
作者：
Matsui, Hotaka
Sopko, Nikolai A.
Hannan, Johanna L.
Bivalacqua, Trinity J.
机构：
[1] Johns Hopkins Sch Med, James Buchanan Brady Urol Inst, Baltimore, MD USA
[2] Johns Hopkins Sch Med, Dept Urol, Baltimore, MD USA
来源：
CURRENT DRUG TARGETS | 2015年 / 16卷 / 05期
基金：
英国医学研究理事会;
关键词：
Angiotensin; erectile dysfunction; nitric oxide; pathophysiology; reactive oxygen species; RhoA/Rho-associated protein kinase; tumor necrosis factor-alpha; NITRIC-OXIDE SYNTHASE; MAJOR PELVIC GANGLION; CAVERNOUS NERVE INJURY; BLADDER OUTLET OBSTRUCTION; URINARY-TRACT SYMPTOMS; VIVO GENE-THERAPY; SEXUAL DYSFUNCTION; CORPUS CAVERNOSUM; ENDOTHELIAL DYSFUNCTION; SMOOTH-MUSCLE;
D O I：
10.2174/138945011605150504114041
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
Erectile dysfunction (ED) is a major health problem as the population ages. Basic science research for the last two decades has expanded the knowledge on ED and identified several key molecular changes associated with the pathogenesis of ED, including nitric oxide (NO)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) pathway, RhoA/Rho-associated protein kinase (ROCK) signaling pathway, reactive oxygen species (ROS), renin-angiotensin system (RAS) and tumor necrosis factor-alpha (TNF-alpha). The causes of ED are classified into aging, vasculogenic, neurogenic, endocrinological, drug-induced and psychogenic. ED is often associated with systemic diseases, such as diabetes and cardiovascular diseases. In this review, we will review the molecular mechanisms of ED and known mechanisms behind ED associated with systemic diseases.
引用
收藏
页码：411 / 419
页数：9
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