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.
Keywords: Adenosine, nitric oxide, opiorphins, rho kinase, recurrent ischemic priapism treatment, testosterone.
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