ArticleHuman genomics2017
Genetic determinants of clinical heterogeneity of the coronary artery disease in the population of Hyderabad, India.
Article in Human genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 20 citations in OpenAlex.
- Multivariate Genome-Wide Association Analysis Identifies Genetic Susceptibility Loci for Metabolic Syndrome in the Korean Genome and Epidemiology Study.International journal of molecular sciences · 2026Article
- Genome-wide association and MaODR-based multi-locus interaction analyses reveal a susceptibility gene network for newly identified metabolic syndrome.Genome biology · 2026Article
- The mechanism of BUD13 m6A methylation mediated MBNL1-phosphorylation by CDK12 regulating the vasculogenic mimicry in glioblastoma cells.Cell death & disease · 2022Article
- Polymorphisms of the 11q23.3 Locus Affect the Risk and Mortality of Coronary Artery Disease.Journal of clinical medicine · 2022Article
- Analysis of 61 SNPs from the CAD specific genomic loci reveals unique set of SNPs as significant markers in the Southern Indian population of Hyderabad.BMC cardiovascular disorders · 2022Article
- Kernel machine SNP set analysis finds the association of BUD13, ZPR1, and APOA5 variants with metabolic syndrome in Tehran Cardio-metabolic Genetics Study.Scientific reports · 2021Article
- The SNP rs7865618 of 9p21.3 locus emerges as the most promising marker of coronary artery disease in the southern Indian population.Scientific reports · 2020Article
- Article
- Genetics, coronary artery disease, and myocardial revascularization: will novel genetic risk scores bring new answers?Indian journal of thoracic and cardiovascular surgery · 2018Review
- Prediction of cholesterol ratios within a Korean population.Royal Society open science · 2018Article
- Interactions of six SNPs in APOA1 gene and types of obesity on low HDL-C disease in Xinjiang pastoral area of China.Lipids in health and disease · 2017Article
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3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundGenetic predisposition to the clinical categories of coronary artery disease (anatomical viz., insignificant, single, double, and triple vessel diseases and phenotypic severity categories viz., angina, acute coronary syndrome, and myocardial infarction) is poorly understood. Particularly, the apolipoprotein genes clustered at 11q23.3 chromosomal region play a vital role in cholesterol homeostasis, and a large number of SNPs identified in this region need to be explored for their association with the clinical categories of CAD.
methodsUsing fluidigm SNP genotyping platform, a prioritized set of 96 SNPs of 11q23.3 chromosomal region were genotyped on 508 CAD cases and 516 ethnicity matched controls, enrolled from Hyderabad, India, and its vicinity.
resultsThe association analysis suggests 19 and 15 SNPs to be significantly associated (p ≤ 0.05) with at least one of the anatomical and/or phenotypic severity categories, respectively. Overall, the six SNPs rs17440396:G>A, rs6589566:A>G, rs2849165:G>A, rs10488699:G>A, rs1263163:G>A, and rs1263171:G>A were significant even after correction for multiple testing. Three of these (rs17440396:G>A, rs6589566:A>G, and rs2849165:G>A) that belong to BUD13, ZPR1, and APOA5-APOA4 intergenic regions, respectively, were found to be associated across the anatomical categories of CAD. However, no particular trend in the genotypic odds ratios with the increasing severity was apparent. The association analysis of the variants with phenotypic severity categories suggests that a high degree of phenotypic severity could be a result of more number of risk alleles. While the risk score analysis suggests high discriminative power of the variants towards the individual clinical categories of CAD, the complex network of interactions seen between the intronic variants of BUD13 and ZPR1 regulatory genes and intergenic variants of APOA5-APOA4 suggests pleiotropic effects of regulatory genes in the manifestation of these CAD categories.
conclusionThe complex network of interactions observed in the present study between the regulatory and protein-coding genes suggests their role in the manifestation of distinct clinical categories of CAD, which needs to be functionally validated.
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