| Description: |
Background: The burden of erectile dysfunction (ED) is rising worldwide due to unresponsiveness of some affected individuals to existing drugs and treatment strategies. Fortunately, improvement in biological techniques has led to the understanding that some cases of the disorder may have a genetic etiology, which, when fully understood, may lead to improved treatment. Objective: This review articulated established ED candidate genes and pathophysiology to assist researchers and medical practitioners to formulate effective drugs and treatment procedures. Methods: The Google search engine was used to retrieve relevant information on the topic from reputable academic databases, including PubMed, Medline, Google Scholar, Scopus, and SpringerLink. Results: The search discovered 10 ED candidate genes, which are SIM1, SLC6A4, 5-HTTLPR, TGFB1, DAT1, MC4R, NOS3, GNB3, AR, and MTHFR. Polymorphisms or mutations in these genes may disrupt erectile activities of the hypothalamus, neurotransmitters such as dopamine, serotonin, and nitric oxide as well as relaxation of penile tissues. Clinical presentations of ED include loss of erection, weak vaginal penetration, premature ejaculation, and anejaculation. Each gene has a distinct mechanism, which, if targeted in the affected may reverse the disorder or reduce the effects. Conclusion: Some cases of ED are genetic, which, when fully understood, may give an insight into new treatment procedures or improve on the current ones. Medical practitioners are advised to formulate treatment procedures that target the affected gene (s) in individuals. |