Association of ET1 and APE1 Genes Polymorphism with Coronary Artery Disease

Syed T Raza1, Ale Eba1, Irshad A Wani2

  • 1Department of Biochemistry, Era's Lucknow Medical College and Hospital Lucknow, Uttar Pradesh, India.

Insights

Genetic variations in the ET1 and APE1 genes were not linked to an increased risk of coronary artery disease (CAD). This study found no significant association between these specific gene polymorphisms and CAD susceptibility in the studied population.

Area of Science:

  • Cardiovascular Genetics
  • Molecular Epidemiology
  • Disease Susceptibility

Background:

  • Coronary artery disease (CAD) is a leading global cause of mortality and disability.
  • CAD arises from complex interactions between genetic and environmental factors, often exhibiting a polygenic architecture.

Purpose of the Study:

  • To investigate the association between Endothelin 1 (ET1) and Apolipoprotein E (APE1) gene polymorphisms and the susceptibility to coronary artery disease (CAD).

Main Methods:

  • Genomic DNA was isolated from venous blood samples using the phenol-chloroform extraction method.
  • Restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) was employed to analyze ET1 and APE1 gene polymorphisms.
  • Genotype frequencies of APE1 (AA, AG, GG) and ET1 (GG, GT, TT) were compared between CAD cases and control groups.

Main Results:

  • The frequencies of APE1 genotypes (AA, AG, GG, AG+GG) in CAD cases were 13.91%, 40.87%, 45.22%, and 86.99%, versus 13%, 50%, 37%, and 87% in controls.
  • The frequencies of ET1 genotypes (GG, GT, TT, GT+TT) in CAD cases were 6.67%, 37.5%, 55.8%, and 93.34%, versus 6.67%, 25.33%, 68%, and 93.34% in controls.
  • No statistically significant association was found between ET1 or APE1 gene polymorphisms and the risk of developing CAD.

Conclusions:

  • The studied polymorphisms in the ET1 and APE1 genes do not appear to be significant risk factors for coronary artery disease.
  • Further research with larger cohorts and diverse populations may be warranted to fully elucidate the role of these genes in CAD pathogenesis.

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