ArticleGenome biology2019
Integrative analysis of vascular endothelial cell genomic features identifies AIDA as a coronary artery disease candidate gene.
Article in Genome biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed.
- 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
- Proteomic Profiling of Endothelial Cells Under Laminar Shear Stress Confirms the Importance of KLF4 in the Regulation of Membrane Protein Expression Compared to Oscillatory Flow.Journal of proteome research · 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
- Functionally informed cis and trans proteome-wide association studies prioritize disease-critical genes.Research square · 2026Article
- Functionally informed cis and trans proteome-wide association studies prioritize disease-critical genes.medRxiv : the preprint server for health sciences · 2026Article
- Functional Genomics Link REST to Endothelial Plasticity and Atherosclerosis.Circulation research · 2026Article
- Single-cell transcriptomic analyses of skin vascular endothelial cells in sedentary and voluntary wheel running young mice.Physiological reports · 2025Article
- Chronic cerebral hypoperfusion induces venous dysfunction via EPAS1 regulation in mice.Nature communications · 2025Article
- RobusTAD: reference panel based annotation of nested topologically associating domains.Genome biology · 2025Article
- Article
- Connecting intermediate phenotypes to disease using multi-omics in heart failure.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2025Article
- Connecting intermediate phenotypes to disease using multi-omics in heart failure.medRxiv : the preprint server for health sciences · 2024Article
- Gene editing therapy for cardiovascular diseases.MedComm · 2024Review
- Coronary Artery Disease Risk Variant Dampens the Expression of CALCRL by Reducing HSF Binding to Shear Stress Responsive Enhancer in Endothelial Cells In Vitro.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction.International journal of molecular sciences · 2024Article
- Mechanosensitive super-enhancers regulate genes linked to atherosclerosis in endothelial cells.The Journal of cell biology · 2024Article
- Review
- Single-nucleus multiregion transcriptomic analysis of brain vasculature in Alzheimer's disease.Nature neuroscience · 2023Article
- The angiopoietin receptor Tie2 is atheroprotective in arterial endothelium.Nature cardiovascular research · 2023Article
- Introducing Circulating Vasculature-Related Transcripts as Biomarkers in Coronary Artery Disease.Molecular diagnosis & therapy · 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
11 authors.
Funding
Abstract
backgroundGenome-wide association studies (GWAS) have identified hundreds of loci associated with coronary artery disease (CAD) and blood pressure (BP) or hypertension. Many of these loci are not linked to traditional risk factors, nor do they include obvious candidate genes, complicating their functional characterization. We hypothesize that many GWAS loci associated with vascular diseases modulate endothelial functions. Endothelial cells play critical roles in regulating vascular homeostasis, such as roles in forming a selective barrier, inflammation, hemostasis, and vascular tone, and endothelial dysfunction is a hallmark of atherosclerosis and hypertension. To test this hypothesis, we generate an integrated map of gene expression, open chromatin region, and 3D interactions in resting and TNFα-treated human endothelial cells.
resultsWe show that genetic variants associated with CAD and BP are enriched in open chromatin regions identified in endothelial cells. We identify physical loops by Hi-C and link open chromatin peaks that include CAD or BP SNPs with the promoters of genes expressed in endothelial cells. This analysis highlights 991 combinations of open chromatin regions and gene promoters that map to 38 CAD and 92 BP GWAS loci. We validate one CAD locus, by engineering a deletion of the TNFα-sensitive regulatory element using CRISPR/Cas9 and measure the effect on the expression of the novel CAD candidate gene AIDA.
conclusionsOur data support an important role played by genetic variants acting in the vascular endothelium to modulate inter-individual risk in CAD and hypertension.
Indexed as
Identifiers
What OpenQuestion holds
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.