Pathophysiology of erectile dysfunction

Hotaka Matsui, Nikolai A. Sopko, Johanna L. Hannan, Trinity J. Bivalacqua

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


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-α). The causes of ED are classified into aging, vasculogenic, neuroenic, 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.

Original languageEnglish (US)
Pages (from-to)411-419
Number of pages9
JournalCurrent Drug Targets
Issue number5
StatePublished - May 1 2015


  • Angiotensin
  • Erectile dysfunction
  • Nitric oxide
  • Pathophysiology
  • Reactive oxygen species
  • RhoA/Rho-associated protein kinase
  • Tumor necrosis factor-alpha

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Drug Discovery
  • Clinical Biochemistry


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