ArticleMolecular biology reports2012
Lack of association between Glu298Asp polymorphism and coronary artery disease in North Indians.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 2 syntheses or guidelines pooled it, 10 citations in OpenAlex.
- Ancestry- and Age-Dependent Effects of NOS3 Polymorphisms on Coronary Heart Disease Risk: A Meta-analysis.Cardiovascular toxicology · 2025Pooled it
- Pooled it
- Association of Endothelial Nitric Oxide Synthase Gene Polymorphisms with Coronary Artery Disease in North Indian Punjabi Population.Biochemical genetics · 2022Article
- Article
- Role of sGC-dependent NO signalling and myocardial infarction risk.Journal of molecular medicine (Berlin, Germany) · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric Oxide (NO) is an important molecule carrying number of different functions in humans. Published studies suggest that it may inhibit several key steps involved in the pathogenesis of atherosclerosis. Inhibition or reduction of NO due to Glu298Asp polymorphism may accelerate atherosclerosis. The aim of this study was to determine whether Glu298Asp polymorphism is implicated in the pathogenesis of coronary artery disease (CAD) among North Indian population from the state of Uttar Pradesh, India. We selected 253 CAD patients and 174 healthy, normotensive, non-diabetic controls, which were matched for gender and ethnicity. The Glu298Asp (rs1799983) variant was detected by genotyping subjects, using a polymerase chain reaction followed by restriction fragment length polymorphism. There was no significant difference found in the genotypic and allelic frequencies between patients and controls. Our study indicated that Glu298Asp polymorphism does not play any critical role in the pathogenesis of CAD, at least in North Indian population.
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Registered trials
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