ArticlePLoS genetics2023
Multimodal CRISPR perturbations of GWAS loci associated with coronary artery disease in vascular endothelial cells.
Article in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Comparing bulk and single-cell methodologies and models to profile gene expression, chromatin accessibility and regulatory links in endothelial cells treated with TNFα.Biochemistry and biophysics reports · 2026Article
- From GWAS Signals to Molecular Mechanisms: Explainable AI for Causal Gene Prioritization and Biomolecular Target Interpretation.Biomolecules · 2026Review
- Cardiovascular Genetic Epidemiology in the Genome-Wide Era: From Association Discovery to Mechanistic Dissection and Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Common Coronary Artery Disease Risk Variants in Endothelial Regulatory Elements Modulate Tetraspanin 14 Expression and Notch Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Comparing bulk and single-cell methodologies and models to profile gene expression, chromatin accessibility and regulatory links in endothelial cells treated with TNFα.bioRxiv : the preprint server for biology · 2026Article
- Mapping functional non-coding variation in individual human genomes through haplotyping, multiomics, and deep learning.Nature communications · 2026Article
- Review
- Decoding Vascular Cell Diversity: Single-Cell Approaches to Mechanisms of Vascular Disease.Circulation research · 2026Review
- Appraisal of CRISPR Technology as an Innovative Screening to Therapeutic Toolkit for Genetic Disorders.Molecular biotechnology · 2026Review
- GWAS-informed data integration and non-coding CRISPRi screen illuminate genetic etiology of bone mineral density.Genome biology · 2025Article
- Article
- A replication study of novel fetal hemoglobin-associated genetic variants in sickle cell disease-only cohorts.Human molecular genetics · 2025Article
- GWAS-Informed data integration and non-coding CRISPRi screen illuminate genetic etiology of bone mineral density.bioRxiv : the preprint server for biology · 2024Article
- Evaluation of Plasma E-Selectin Concentration as a Risk Marker for Atherosclerotic Vascular Damage in Patients with Early CAD.Biomolecules · 2024Article
- Human genetics and epigenetics of alcohol use disorder.The Journal of clinical investigation · 2024Review
- SpRY-mediated screens facilitate functional dissection of non-coding sequences at single-base resolution.Cell genomics · 2024Article
- Investigating mobile element variations by statistical genetics.Human genome variation · 2024Review
- Article
- Protein interaction networks in the vasculature prioritize genes and pathways underlying coronary artery disease.Communications biology · 2024Article
- High-throughput PRIME-editing screens identify functional DNA variants in the human genome.Molecular cell · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Genome-wide association studies have identified >250 genetic variants associated with coronary artery disease (CAD), but the causal variants, genes and molecular mechanisms remain unknown at most loci. We performed pooled CRISPR screens to test the impact of sequences at or near CAD-associated genetic variants on vascular endothelial cell functions. Using CRISPR knockout, inhibition and activation, we targeted 1998 variants at 83 CAD loci to assess their effect on three adhesion proteins (E-selectin, ICAM1, VCAM1) and three key endothelial functions (nitric oxide and reactive oxygen species production, calcium signalling). At a false discovery rate ≤10%, we identified significant CRISPR perturbations near 42 variants located within 26 CAD loci. We used base editing to validate a putative causal variant in the promoter of the FES gene. Although a few of the loci include genes previously characterized in endothelial cells (e.g. AIDA, ARHGEF26, ADAMTS7), most are implicated in endothelial dysfunction for the first time. Detailed characterization of one of these new loci implicated the RNA helicase DHX38 in vascular endothelial cell senescence. While promising, our results also highlighted several limitations in using CRISPR perturbations to functionally dissect GWAS loci, including an unknown false negative rate and potential off-target effects.
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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.