ArticleHuman genomics2022
Enhancer promoter interactome and Mendelian randomization identify network of druggable vascular genes in coronary artery disease.
Article in Human genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Mitochondria-Related Genome-Wide Mendelian Randomization Identifies Putatively Genes for Chronic Fatigue.Molecular neurobiology · 2026Article
- IL3RA identified as novel biomarker and therapeutic target for ERClinical proteomics · 2026Article
- Genetic link between metabolic syndrome and coronary artery disease: Insights from genome-wide cross-trait analysis.Global medical genetics · 2026Article
- Discover QTLs for the level of blood components in Shaoxing duck using GWAS and haplotype sharing analysis.Animal biotechnology · 2024Article
- Mendelian randomization reveals interactions of the blood proteome and immunome in mitral valve prolapse.Communications medicine · 2024Article
- Integrative approaches based on genomic techniques in the functional studies on enhancers.Briefings in bioinformatics · 2023Review
- Review
- Identification of immune-related genes in diagnosing atherosclerosis with rheumatoid arthritis through bioinformatics analysis and machine learning.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Coronary artery disease (CAD) is a multifactorial disorder, which is partly heritable. Herein, we implemented a mapping of CAD-associated candidate genes by using genome-wide enhancer-promoter conformation (H3K27ac-HiChIP) and expression quantitative trait loci (eQTL). Enhancer-promoter anchor loops from human coronary artery smooth muscle cells (HCASMC) explained 22% of the heritability for CAD. 3D enhancer-promoter genome mapping of CAD-genes in HCASMC was enriched in vascular eQTL genes. By using colocalization and Mendelian randomization analyses, we identified 58 causal candidate vascular genes including some druggable targets (MAP3K11, CAMK1D, PDGFD, IPO9 and CETP). A network analysis of causal candidate genes was enriched in TGF beta and MAPK pathways. The pharmacologic inhibition of causal candidate gene MAP3K11 in vascular SMC reduced the expression of athero-relevant genes and lowered cell migration, a cardinal process in CAD. Genes connected to enhancers are enriched in vascular eQTL and druggable genes causally associated with CAD.
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Registered trials
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