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Association between previously identified loci affecting telomere length and coronary heart disease (CHD) in Han
Hui Ding1, Fen Yan1, Lin-Lin Zhou2
1Department of Pulmonary Medicine, The Affiliated Yixing People's Hospital, Jiangsu University, Zhenjiang, Jiangsu Province, People's Republic of China.
Insights
The NAF1 gene rs7675998 single nucleotide polymorphism (SNP) is associated with coronary heart disease (CHD) risk and earlier onset age in the Chinese Han population. This finding supports telomere biology
Area of Science:
- Genetics
- Cardiovascular Disease
- Telomere Biology
Background:
- Telomere length is associated with cellular aging and various diseases, including coronary heart disease (CHD).
- Previous studies identified single-nucleotide polymorphisms (SNPs) linked to telomere length.
- Replication in diverse populations is crucial for validating genetic associations.
Purpose of the Study:
- To replicate previously identified telomere-length loci in a Chinese Han population with CHD.
- To investigate the association of these loci with CHD susceptibility and age at onset.
Main Methods:
- Genotyping of 1514 CHD patients and 2470 controls for seven telomere-length SNPs (rs10936599, rs2736100, rs7675998, rs9420907, rs8105767, rs755017, rs11125529).
- Collection of clinical data including age, sex, BMI, lipids, hypertension, diabetes, and dyslipidemia.
- Statistical analysis including Hardy-Weinberg equilibrium, genotype/allele frequencies, odds ratios, and ANOVA for age at onset.
Main Results:
- The SNP rs7675998 in the NAF1 gene showed significant differences in genotype and allele frequencies between CHD patients and controls.
- Carriage of the A allele of rs7675998 was associated with a 2.127-fold increased odds of CHD.
- The AA genotype of rs7675998 was significantly associated with an earlier age at onset of CHD.
Conclusions:
- The NAF1 gene, specifically the rs7675998 polymorphism, may influence both the susceptibility to and the age at onset of coronary heart disease in the Chinese Han population.
- These findings align with previous reports from European studies, suggesting a conserved role for NAF1 in CHD pathogenesis.
- Telomere biology markers warrant further investigation as potential risk factors for cardiovascular disease.
Purpose:
To replicate previously confirmed telomere-length loci in a Chinese Han population with coronary heart disease (CHD), and investigate these loci and the possibility of and age at onset of CHD.
Patients And Methods:
1514 CHD patients and 2470 normal controls were recruited. Medical data including age, sex, body mass index, lipid profiles, history of hypertension, type 2 diabetes mellitus, and dyslipidemia were collected from all the participants. Seven previously identified single-nucleotide polymorphisms (SNPs) related to leucocyte telomere length were genotyped, including rs10936599 in TERC, rs2736100 in TERT, rs7675998 in NAF1, rs9420907 in OBFC1, rs8105767 in ZNF208, rs755017 in RTEL1, and rs11125529 in ACYP2.
Results:
No significant difference in genotype frequencies from the Hardy-Weinberg equilibrium test was noted for all tested SNPs both in the CHD patients and the normal controls. No polymorphism was observed for rs9420907, and AA genotype was noted in both the CHD patients and the controls. Neither the genotype nor the allele frequencies of rs2736100, rs8105767, rs11125529, and rs2967374 were significantly different between the CHD patients and the normal controls. For rs10936599 and rs755017, statistical difference was found for the allele frequency but not genotype. Distributions of genotype and allele were significantly different between the two groups for rs7675998. The odds ratio for carriers of CHD was 2.127 (95% confidence interval: 1.909-2.370) for the A allele of rs7675998. By one-way analysis of variance test, rs7675998 was associated with the onset age of CHD. CHD patients with the AA genotype of rs7675998 had significantly lower onset age (P<0.05).
Conclusion:
In a Chinese Han population, NAF1 gene encoding proteins with known function in telomere biology may influence both the possibility of and the age at onset of CHD, as previously reported in European studies.
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