ArticleGenetic epidemiology2022
Interaction between genetics and smoking in determining risk of coronary artery diseases.
Article in Genetic epidemiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Coronary artery disease in smokers with low traditional risk burden: An exploratory analysis of potential genetic susceptibility.Journal of molecular and cellular cardiology plus · 2026Article
- Smoking-Associated Changes in Gene Expression in Coronary Artery Disease Patients Using Matched Samples.Current issues in molecular biology · 2024Article
- Integrating GWAS summary statistics, individual-level genotypic and omic data to enhance the performance for large-scale trait imputation.Human molecular genetics · 2023Article
- Epidemiological analysis of coronary heart disease and its main risk factors: are their associations multiplicative, additive, or interactive?Annals of medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Coronary artery disease (CAD) is a preeminent cause of death, and smoking is a strong risk factor for CAD. Genetic factors contribute to the development of CAD, but the interplay between genetic predisposition and smoking history in CAD remains unclear. Using data from the UK Biobank, we constructed several genetic risk scores (GRSs) based on known CAD loci and assessed their interactions with smoking for the development of incident CAD in 307,147 participants of European ancestry who were free of CAD. We fitted Cox proportional hazard models and assessed gene-smoking interaction on both multiplicative and additive scales. Overall, we found no multiplicative interactions, but observed a synergistic additive interaction of GRS with both smoking status and pack-years of smoking, finding that the absolute CAD risk due to smoking was higher for those with high genetic risk. Trait-based sub-GRSs suggested smoking status and smoking intensity measured by pack-years might confer gene-smoking interaction effects with different intermediate risk factors for CAD. Our study results suggest that genetics could modify the effects of smoking on CAD and highlight the value of addressing gene-lifestyle interactions on both additive and multiplicative scales.
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Registered trials
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