Molecular Pathophysiology of Priapism: Emerging Targets

被引:23
作者
Anele, Uzoma A. [1 ,2 ]
Morrison, Belinda F. [3 ]
Burnett, Arthur L. [1 ,2 ]
机构
[1] Johns Hopkins Univ, Sch Med, James Buchanan Brady Urol Inst, Baltimore, MD 20817 USA
[2] Johns Hopkins Univ, Sch Med, Dept Urol, Baltimore, MD 20817 USA
[3] Univ W Indies, Dept Surg, Mona, Jamaica
关键词
Adenosine; nitric oxide; opiorphins; rho kinase; recurrent ischemic priapism treatment; testosterone; SICKLE-CELL-DISEASE; NITRIC-OXIDE SYNTHASE; RECURRENT ISCHEMIC PRIAPISM; TESTOSTERONE INDUCED PRIAPISM; ERECTILE FUNCTION; ADENOSINE-DEAMINASE; STUTTERING PRIAPISM; CORPUS CAVERNOSUM; INHIBITOR THERAPY; EXCESS ADENOSINE;
D O I
10.2174/1389450115666141111111842
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Priapism is an erectile disorder involving uncontrolled, prolonged penile erection without sexual purpose, which can lead to erectile dysfunction. Ischemic priapism, the most common of the variants, occurs with high prevalence in patients with sickle cell disease. Despite the potentially devastating complications of this condition, management of recurrent priapism episodes historically has commonly involved reactive treatments rather than preventative strategies. Recently, increasing elucidation of the complex molecular mechanisms underlying this disorder, principally involving dysregulation of nitric oxide signaling, has allowed for greater insights and exploration into potential therapeutic targets. In this review, we discuss the multiple molecular regulatory pathways implicated in the pathophysiology of priapism. We also identify the roles and mechanisms of molecular effectors in providing the basis for potential future therapies.
引用
收藏
页码:474 / 483
页数:10
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