What is it about?

To investigate the association between G-protein β3 (GNB3) subunit gene 825C/T polymorphism and vasculogenic ED (VED).

Featured Image

Why is it important?

Penile arterial insufficiency is one of the most common causes of erectile dysfunction (ED). Atherosclerotic occlusive disease can decrease arterial flow to the corpus cavernosum sinusoidal spaces, thus impairing penile tumescence. Common risk factors associated with general atherosclerosis include hypertension, hyperlipidemia, diabetes mellitus, and cigarette smoking. The 825T allele is associated with increased signal transduction . This polymorphism has been shown to be associated with hypertension, therosclerosis, obesity, and insulin resistance. Total cholesterol is significantly higher in subjects with the T allele. In a pilot study, Sperling et al. reported that homozygous 825T allele carriers had an improved erectile response to sildenafil. Taking into consideration the known influence of the 825C/T polymorphism on vascular risk factors for ED, this investigation was performed to test the hypothesis that the presence of the 825T allele of the GNB3 gene results in an increased risk of vasculogenic ED (VED).

Perspectives

Phosphodiesterase-5 inhibitors present the first orally effective symptomatic treatment of ED. However, we are still far from curing ED. To bring us closer to curing VED, we need to better clarify the underlying mechanisms of VED. In addition to known risk factors, genetic risk factors may have essential roles in the pathogenesis of ED. Determination of these genetic risk factors is expected to improve our understanding of the molecular basis for ED.

Dr Mohammad Reza Safarinejad
University of Medical Sceices

Read the Original

This page is a summary of: G-protein β3 subunit gene 825C/T polymorphism and its association with the presence, severity, and duration of vasculogenic erectile dysfunction, Fertility and Sterility, January 2013, Elsevier,
DOI: 10.1016/j.fertnstert.2012.08.033.
You can read the full text:

Read

Resources

Contributors

The following have contributed to this page