Related Experiment Video

Updated: Jun 29, 2026

Treatment Model for Young Patients with Psychogenic Erectile Dysfunction and Resultant Infertility
04:22

Treatment Model for Young Patients with Psychogenic Erectile Dysfunction and Resultant Infertility

Published on: May 30, 2025

[Single base polymorphisms and erectile dysfunction]

A Eisenhardt1, H Rübben, H Sperling

  • 1Urologische Klinik, Kliniken Maria Hilf GmbH, Viersener Str. 450, 41063 Mönchengladbach. Andreas.Eisenhardt@mariahilf.de

Der Urologe. Ausg. A
|October 16, 2008
PubMed

Insights

Erectile dysfunction (ED) risk is linked to cardiovascular diseases. Genetic variations called single nucleotide polymorphisms may influence both ED and cardiovascular risk, affecting treatment response.

Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Pharmacology

Context:

  • Erectile dysfunction (ED) shares risk factors with cardiovascular diseases (CVDs), including coronary heart disease, hypertension, hypercholesterolemia, and diabetes.
  • Molecular genetics research is uncovering links between genetic variations and complex diseases.
  • Understanding these links is crucial for personalized medicine.

Purpose:

  • To review current knowledge on the association between single nucleotide polymorphisms (SNPs) and erectile dysfunction.
  • To explore the relationship between SNPs and the response to phosphodiesterase type 5 (PDE-5) inhibitors, such as sildenafil.
  • To highlight the role of genetic factors in ED pathophysiology and treatment.

Summary:

  • Cardiovascular morbidities are strongly associated with an increased risk of erectile dysfunction.
  • Studies show a connection between specific single nucleotide polymorphisms (SNPs) and the risk of developing cardiovascular diseases.
  • This review examines the current evidence linking SNPs to ED and their impact on sildenafil efficacy.

Impact:

  • Provides insights into the genetic underpinnings of erectile dysfunction.
  • May guide the development of targeted diagnostic and therapeutic strategies for ED.
  • Informs clinical practice regarding the use of PDE-5 inhibitors in patients with specific genetic profiles.

Related Concept Videos

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment01:08

Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment

Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors01:28

Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors

Phosphodiesterase 5 (PDE5) inhibitors are potent enzymes that function to hydrolyze cyclic nucleotides to their corresponding 5' monophosphates. Their unique biochemical properties have been applied in treating Pulmonary Arterial Hypertension (PAH).
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Pharmacogenetics of Drug Metabolism: Overview01:27

Pharmacogenetics of Drug Metabolism: Overview

Genetic polymorphism in drug metabolism is crucial to the inter-individual variability observed in drug responses. Drug metabolism primarily involves the chemical modification of drugs and other xenobiotics to enhance their elimination by increasing their polarity. Two main classes of enzymes mediate this biotransformation process: Phase I enzymes, primarily cytochrome P450s, catalyze oxidation and reduction reactions, while other enzymes, such as esterases, mediate hydrolysis, and Phase II...
Principles of Pharmacogenetics: Types of Genetic Variants01:27

Principles of Pharmacogenetics: Types of Genetic Variants

The human genome is over 99.9% identical between individuals, yet genetic differences exist at millions of bases. The human genome contains approximately 3 million variant positions per individual, many of which are heterozygous, contributing to genetic diversity and individual traits. Genetic variations include single-nucleotide polymorphisms (SNPs), insertions, deletions, and copy number variations (CNVs).SNPs, the most common variation, involve single-base changes in DNA. These can be...