ArticleAtherosclerosis2020
Multiple independent mechanisms link gene polymorphisms in the region of ZEB2 with risk of coronary artery disease.
Article in Atherosclerosis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Shared genetic risk factors and causal association between psoriasis and coronary artery disease.Nature communications · 2022Pooled it
- Epigenetic signatures of cardiometabolic risk in men: accelerated aging and differential methylation replicated across cohorts.Clinical epigenetics · 2026Article
- The intersection of disorders of sex development and cardiovascular diseases.Biology of sex differences · 2026Review
- A macrophage gene-regulatory network linked to clinical severity of coronary artery disease : The STARNET and NGS-PREDICT primary blood macrophage studies.Basic research in cardiology · 2025Article
- Integrative gene regulatory network analysis discloses key driver genes of fibromuscular dysplasia.Nature cardiovascular research · 2024Article
- The HDAC9-associated risk locus promotes coronary artery disease by governing TWIST1.PLoS genetics · 2022Article
- The correlation of long non-coding RNAs IFNG-AS1 and ZEB2-AS1 with IFN-γ and ZEB-2 expression in PBMCs and clinical features of patients with coronary artery disease.Molecular biology reports · 2022Article
- Integrative Prioritization of Causal Genes for Coronary Artery Disease.Circulation. Genomic and precision medicine · 2022Article
- The Associated of the Risk of IVIG Resistance in Kawasaki Disease withJournal of inflammation research · 2022Article
- Precision Medicine Approaches to Vascular Disease: JACC Focus Seminar 2/5.Journal of the American College of Cardiology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 4 countries.
Funding
Abstract
BACKGROUND AND
aimsCoronary artery disease (CAD) arises from the interaction of genetic and environmental factors. Although genome-wide association studies (GWAS) have identified multiple risk loci and single nucleotide polymorphisms (SNPs) associated with risk of CAD, they are predominantly located in non-coding or intergenic regions and their mechanisms of effect are largely unknown. Accordingly, our objective was to develop a data-driven informatics pipeline to understand complex CAD risk loci, and to apply this to a poorly understood cluster of SNPs in the vicinity of ZEB2.
methodsWe developed a unique informatics pipeline leveraging a multi-tissue CAD genetics-of-gene-expression dataset, GWAS datasets, and other resources. The pipeline first dissected SNP locations and their linkage disequilibrium relationships, and progressed through analyses of tissue-specific expression quantitative trait loci, and then gene-gene, gene-phenotype, SNP-phenotype relationships. The pipeline concluded by exploring CAD-relevant gene regulatory networks (GRNs).
resultsWe identified three independent CAD risk SNPs in close proximity to the ZEB2 coding region (rs6740731, rs17678683 and rs2252641/rs1830321). Our pipeline determined that these SNPs likely act in concert via the atherosclerotic arterial wall and adipose tissues, by governing metabolic and lipid functions. In addition, ZEB2 is the top key driver of a liver-specific GRN that is related to lipid levels, metabolic and anthropometric measures, and CAD severity.
conclusionsUsing a novel informatics pipeline, we disclosed the multi-faceted mechanisms of action of the ZEB2-associated CAD risk SNPs. This pipeline can serve as a roadmap to dissect complex SNP-gene-tissue-phenotype relationships and to reveal targets for tissue- and gene-specific therapeutic interventions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.