Related Experiment Video
Updated: Apr 13, 2026

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
Published on: June 9, 2018
A coronary artery disease-associated SNP rs6903956 contributed to asymptomatic hyperuricemia susceptibility in Han
Jianfen Meng1,2, Wenfeng Tan3, Yujing Zhu4
1Department of Rheumatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China. jianfenmeng@163.com.
Insights
A specific gene variant (rs6903956) linked to coronary artery disease risk is associated with asymptomatic hyperuricemia in Han Chinese individuals. This finding suggests a genetic connection between hyperuricemia and cardiovascular disease.
Area of Science:
- Genetics
- Cardiovascular Disease Research
- Metabolic Disorders
Background:
- Coronary artery disease (CAD) is a significant health concern.
- Asymptomatic hyperuricemia (aHU) is a condition characterized by elevated uric acid levels without symptoms.
- Investigating genetic predispositions for aHU is crucial for understanding its link to cardiovascular health.
Purpose of the Study:
- To determine the association between the CAD risk single nucleotide polymorphism (SNP) rs6903956 and the susceptibility to asymptomatic hyperuricemia (aHU).
- To explore the potential of rs6903956 as an independent risk factor for aHU in the Han Chinese population.
Main Methods:
- A case-control study involving 221 aHU patients and 447 healthy controls.
- Genotyping of the SNP rs6903956 was performed using TaqMan probe technology.
- Multivariate logistic regression analysis was employed to assess risk factors, adjusting for established CAD risk factors.
Main Results:
- Significant differences in genotype and allele frequencies of rs6903956 were observed between aHU cases and controls (p<0.001).
- The AA genotype of rs6903956 was strongly associated with aHU (OR=8.672, p<0.001).
- rs6903956 was identified as an independent risk factor for aHU susceptibility, even after adjusting for other cardiovascular risk factors.
Conclusions:
- This study provides the first evidence of a genetic link between the CAD-associated SNP rs6903956 and aHU in the Han Chinese population.
- The findings support a close relationship between hyperuricemia and coronary artery disease through shared genetic factors.
- rs6903956 may serve as a potential genetic marker for aHU risk.
Background:
To investigate the association of a coronary artery disease (CAD) risk SNP rs6903956 with asymptomatic hyperuricemia (aHU) susceptibility in Han Chinese.
Methods:
Two hundred and twenty one patients with aHU and 447 healthy controls were recruited for this study. SNP rs6903956 were genotyped using TaqMan probe.
Results:
The overall genotype and allele frequency distribution of the rs6903956 showed significant difference between aHU cases and controls (p<0.001 for genotype and allele, respectively). AA genotype of rs6903956 was significantly associated with aHU (OR=8.672, 95% CI 2.811-26.753, p<0.001) in our Han Chinese aHU cohort. Multivariate logistic regression analysis indicated that rs6903956 might be an independent risk factor for aHU susceptibility (OR=10.642 [2.671-42.400], p=0.001 for codominant model and OR=9.205 [2.336-36.280], p=0.002 for recessive model) after adjustment for some well- known CAD risk factors including age, gender, body mass index, smoking, hypertension, diabetes mellitus, abnormal glycometabolism, lipid abnormality and alcohol intake. No significant genotype-specific difference in uric acid levels was observed in aHU patients and controls.
Conclusions:
Our findings are the first to establish a genetic link of a CAD-associated rs6903956 with aHU in a Han Chinese population, providing the genetic evidence to support the close relationship between hyperuricemia and CAD.
Related Concept Videos
Single Nucleotide Polymorphisms-SNPs
Genome-wide Association Studies-GWAS
GWAS does not require the identification of the target gene involved in...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu
Pharmacogenomics: Identification of New Drug Targets
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters

