Related Experiment Video

Updated: Jul 6, 2026

Vascular Gene Transfer from Metallic Stent Surfaces Using Adenoviral Vectors Tethered through Hydrolysable Cross-linkers
12:30

Vascular Gene Transfer from Metallic Stent Surfaces Using Adenoviral Vectors Tethered through Hydrolysable Cross-linkers

Published on: August 12, 2014

Heme oxygenase-1 gene promotor microsatellite polymorphism is associated with angiographic restenosis after coronary

Ying-Hwa Chen1, Lee-Young Chau, Ming-Wei Lin

  • 1Division of Cardiology, Department of Internal Medicine, Taipei Veterans General Hospital, 201 Sec. 2 Shih-Pai Road, Taipei 112, Taiwan, ROC.

European Heart Journal
|December 20, 2003
PubMed

Insights

Genetic variations in the HO-1 gene promoter influence restenosis after coronary stenting. Longer GT repeats are linked to increased risks of restenosis and adverse cardiac events, suggesting a genetic predisposition.

Area of Science:

  • Cardiovascular Genetics
  • Molecular Cardiology
  • Biomarkers in Cardiology

Background:

  • Heme oxygenase-1 (HO-1) produces carbon monoxide (CO), which has anti-inflammatory and antiproliferative effects in vascular walls.
  • HO-1 plays a role in neointimal formation post-vascular injury.
  • A length polymorphism in the GT repeat of the human HO-1 gene promoter affects gene transcription levels.

Purpose of the Study:

  • To investigate the association between the length of GT repeats in the HO-1 gene promoter and the risk of restenosis and adverse cardiac events following coronary stenting.
  • To determine if HO-1 gene promoter polymorphism is an independent risk factor for post-stenting complications.

Main Methods:

  • Quantitative coronary angiography performed before, immediately after, and 6 months post-stent implantation in 323 patients.
  • Genotyping for the (GT)(n) repeat length polymorphism in the HO-1 gene promoter for all participants.
  • Statistical analysis including adjusted odds ratios (OR) to assess the association between GT repeat length and clinical outcomes.

Main Results:

  • Patients with longer (GT)(n) repeats (≥26) exhibited significantly higher rates of angiographic restenosis compared to those with shorter repeats (OR=3.74, P=0.002).
  • This association was more pronounced in patients with smaller coronary arteries or complex lesions.
  • Carriers of the long/long (L/L) genotype had a substantially increased risk of adverse cardiac events during follow-up (OR=3.26, P=0.001).

Conclusions:

  • The length polymorphism of the GT repeat in the HO-1 gene promoter is an independent risk factor for both angiographic restenosis and adverse cardiac events after coronary stenting.
  • These findings highlight a genetic contribution to stent restenosis.
  • Longer GT repeats may impair HO-1 gene transcription, reducing vascular protection against injury.
Abstract

More Related Videos

A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene07:00

A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene

Published on: April 1, 2019

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty10:03

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty

Published on: January 28, 2020

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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...
Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters01:16

Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters

The pharmacogenetics of drug transporters is increasingly recognized as a critical factor influencing interindividual variability in drug absorption, distribution, and elimination. These membrane-bound proteins regulate drugs' movement across cellular barriers by actively pumping them out (efflux) or facilitating their uptake (influx). Among the major transporter families, ATP-binding cassette (ABC) and solute carrier (SLC) transporters play particularly prominent roles. Genetic polymorphisms...
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...
Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...