Molecular mechanisms associated with diabetic endothelial-erectile dysfunction

被引:125
作者
Castela, Angela [1 ]
Costa, Carla [1 ]
机构
[1] Univ Porto, Dept Biochem, Fac Med, P-4200319 Oporto, Portugal
关键词
NITRIC-OXIDE SYNTHASE; ADVANCED GLYCATION ENDPRODUCTS; PROGENITOR-CELL MOBILIZATION; GROWTH-FACTOR; OXIDATIVE STRESS; CORPUS CAVERNOSUM; ANDROGEN RECEPTOR; GLYCEMIC CONTROL; REACTIVE OXYGEN; TESTOSTERONE DEFICIENCY;
D O I
10.1038/nrurol.2016.23
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Erectile dysfunction (ED) is a common complication of diabetes, affecting up to 75% of all diabetic men. Although the aetiology of diabetic ED is multifactorial, endothelial dysfunction is recognized as a mainstay in the pathophysiology of the disease. Endothelial dysfunction is induced by the detrimental actions of high glucose levels and increased oxidative stress on endothelial cells that make up the vascular lining. Besides directly injuring the endothelium, diabetes might also hamper vascular repair mechanisms of angiogenesis and vasculogenesis. These states exacerbate and maintain endothelial dysfunction, impairing vasorelaxation events and cavernosal blood perfusion, which are crucial for normal erectile function.
引用
收藏
页码:266 / 274
页数:9
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