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Association of NF-κB1 gene polymorphisms with coronary artery disease in a Han Chinese population

X L Guo1, X C Liu1, G B Su1

  • 1Department of Cardiothoracic Surgery, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, China.

Genetics and Molecular Research : GMR
|August 16, 2016
PubMed

Insights

Genetic variations in the Nuclear Factor kappa B 1 (NF-κB1) gene are linked to increased susceptibility to coronary artery disease (CAD). Specifically, the rs28362491 polymorphism in the NF-κB1 gene is associated with higher CAD risk.

Area of Science:

  • Genetics
  • Cardiology
  • Molecular Biology

Background:

  • Nuclear factor kappa B 1 (NF-κB1) is a transcription factor crucial for cell functions, including immunity.
  • Activated NF-κB1 and its genetic variations are implicated in the development of coronary artery disease (CAD).

Purpose of the Study:

  • To investigate the association between single nucleotide polymorphisms (SNPs) in the NF-κB1 gene and genetic susceptibility to CAD.
  • To identify specific NF-κB1 gene markers contributing to CAD risk.

Main Methods:

  • Genotyping of seven NF-κB1 gene SNPs (rs28362491, rs230531, rs230528, rs1005819, rs4648055, rs3774964, rs3774968) using the SNaPshot assay.
  • Comparative analysis of genotype and allele frequencies between 361 CAD patients and 385 healthy controls.
  • Linkage disequilibrium and haplotype analyses were performed.

Main Results:

  • Significant differences in genotype and allele frequencies for the rs28362491 (promoter region) polymorphism were observed between CAD patients and controls.
  • The 'D' allele of rs28362491 was found at a significantly higher frequency in CAD patients (P = 0.005 after Bonferroni correction).
  • Strong linkage disequilibrium was noted in one block, but NF-κB1 haplotypes in this block did not show significant risk or protective effects.

Conclusions:

  • NF-κB1 gene polymorphisms, particularly rs28362491, are associated with increased susceptibility to coronary artery disease.
  • These findings support the role of NF-κB1 dysfunction in the pathophysiology of CAD.
  • The study highlights specific genetic markers that may contribute to CAD risk.

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