A single nucleotide polymorphism in the stromal cell-derived factor 1 gene is associated with coronary heart disease

Lei Feng1, Shi-Yan Nian2, Ying-Lu Hao3

  • 1Department of Laboratory Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. fengleii@kmmu.edu.cn.

Insights

Genetic variations in the stromal cell-derived factor 1 (SDF-1) gene are linked to coronary heart disease (CHD). The GG genotype of rs1801157 is an independent risk factor for CHD in the Chinese population.

Area of Science:

  • Genetics
  • Cardiovascular Disease
  • Molecular Biology

Background:

  • Coronary heart disease (CHD) is a leading global cause of mortality.
  • Genetic predisposition is a significant non-modifiable risk factor for CHD.
  • The stromal cell-derived factor 1 (SDF-1) gene plays a role in cardiovascular health.

Purpose of the Study:

  • To investigate the association between a specific single nucleotide polymorphism (SNP) in the SDF-1 gene (rs1801157) and the risk of CHD.
  • To identify genetic and clinical risk factors for CHD in a Chinese population.

Main Methods:

  • Recruited 84 Chinese patients with CHD and 253 healthy controls.
  • Genotyped the SDF-1 rs1801157 polymorphism.
  • Utilized multivariate logistic regression analysis to evaluate associations with CHD.

Main Results:

  • The GG genotype of SDF-1 rs1801157 was significantly more frequent in the CHD group (59.5%) compared to controls (49.8%) (p=0.036).
  • The GG genotype was identified as an independent risk factor for CHD (OR=2.31, 95% CI=1.21-5.23).
  • Male sex, advanced age, hypertension, and elevated LDL-C, low HDL-C, and high TG levels were also independent risk factors.

Conclusions:

  • The GG genotype of the SDF-1 rs1801157 polymorphism is associated with an increased risk of coronary heart disease in the studied Chinese population.
  • This genetic variant, along with established clinical factors, contributes to CHD development.
  • Further research may elucidate the functional mechanisms linking SDF-1 variants to CHD pathogenesis.

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