一氧化氮及其信号转导通路在糖尿病性勃起功能障碍的作用  

Role of Nitric Oxide and its Signal Transduction Pathway in Diabetic Erectile Dysfunction

作　　者：钟梅芳 丁文龙[1] 

机构地区：[1]上海交通大学医学院解剖学教研室,上海200025

出　　处：《解剖科学进展》2007年第1期83-86,90,共5页Progress of Anatomical Sciences

基　　金：上海市自然科学基金资助项目(No.03ZR14042)

摘　　要：勃起功能障碍(erectile dysfunction,ED)是糖尿病的常见并发症,影响人们的生活质量,其病变机理还不甚清楚。一氧化氮(NO)由一氧化氮合酶(NOS)合成,是调节海绵体肌肉松弛和阴茎勃起的重要的神经递质。PI3-kinase/Akt(PKB)通路使eNOS磷酸化,NO的产量增加;NO/cGMPPKG通路参与平滑肌的舒张;RhoA和Rho-kinase参与平滑肌的收缩,抑制eNOS基因表达和酶的活性。周围血管病变和自主神经变性是引起糖尿病性ED的主要原因之一。基因和干细胞(eNOS、RhoA/Rho-kinase与Mesenchymal stem cell-based cell)治疗糖尿病性ED取得一些进展。Erectile dysfunction （ED） is a common complication of diabetes and a cause of decreased quality of life. The specific causes of erectile dysfunction are unknown. Among the neurotransmitters involved in corpus cavernosum smooth muscle relaxation, nitric oxide （NO） synthesized by nitric oxide synthase plays an essential role in ensuring normal penile erection, eNOS is activated by viscous drag/shear stress in blood vessels to produce NO continuously, a process mediated by the phosphatidylinositol 3-kinase （PI3-kinase）/Akt physiologically mediates erection. Relaxation of smooth muscle is primarily mediated by NO/cGMP/PKG pathway, contraction of smooth muscle is primarily mediated by RhoA/Rho-kinase pathway, which suppresses eNOS gene expression and enzyme activity. The mechanisms leading to diabetes - associated ED involve peripheral vasculopathy and autonomic neuropathyo Adenoviral-mediated intracavemosal transfer of therapeutic genes and stem cells thearapy, such as eNOS and RhoA/Rho-kinase and mesenchymal stem cell-based cell, were performed.

关 键 词：糖尿病性勃起功能障碍 一氧化氮合酶 信号转导通路 ENOS 周围血管病变 基因表达 常见并发症 生活质量 

分 类 号：R587.2[医药卫生—内分泌]