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[The apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease]

Chunhong Wang1, Xin Zhou, Fang Zheng

  • 1Department of Hygiene, School of Medicine, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, 430071 P. R. China. chwang027@yahoo.com.cn

Zhonghua Yi Xue Yi Chuan Xue Za Zhi = Zhonghua Yixue Yichuanxue Zazhi = Chinese Journal of Medical Genetics
|March 29, 2005
PubMed

Insights

Apolipoprotein E (apoE) and apoCI gene variations on chromosome 19 are linked to coronary artery disease (CAD) susceptibility. Their interaction with smoking and alcohol significantly elevates CAD risk.

Area of Science:

  • Genetics
  • Cardiovascular Disease Research
  • Molecular Biology

Context:

  • Coronary artery disease (CAD) is a leading cause of mortality worldwide.
  • Genetic factors play a significant role in CAD development.
  • The apolipoprotein E-CI-CII gene cluster on chromosome 19 is a candidate region for CAD susceptibility.

Purpose:

  • To investigate the association between polymorphisms in the apolipoprotein E (apoE), apoCI, and apoCII genes and the risk of coronary artery disease (CAD).
  • To examine the linkage disequilibrium between these genes and their combined effect with environmental factors on CAD.
  • To identify specific haplotypes and gene-environment interactions contributing to CAD pathogenesis.

Summary:

  • The study identified significantly higher frequencies of apoE E3/4 genotype and epsilon4 allele, as well as apoCI H2 allele, in CAD patients compared to controls.
  • Strong linkage disequilibrium was observed between apoE and apoCI genes.
  • Haplotype analysis revealed an excess of epsilon4-H2-T1 in CAD patients.
  • Multivariate analysis demonstrated a significant multiplicative interaction between the epsilon4 allele, H2 allele, and smoking, and an additive interaction with alcohol consumption, significantly increasing CAD risk.

Impact:

  • This research highlights apoE and apoCI as susceptibility loci for CAD, with their linkage disequilibrium contributing to disease development.
  • The findings underscore the critical role of gene-environment interactions, particularly with smoking and alcohol, in modulating CAD risk.
  • These insights could inform personalized risk assessment and preventive strategies for coronary artery disease.
Abstract

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