ArticleCirculation2022
Article in Circulation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Comprehensive Integration of Multiple Single-Cell Transcriptomic Data Sets Defines Distinct Cell Populations and Their Phenotypic Changes in Murine Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2024Pooled it
- Single-Cell Proteomics Uncovers Cell-Specific Proteins in Vascular Health and Marfan Syndrome Disease-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- ZEB2 SUMOylation in Cardiac Fibroblast Drives Post-Infarction Cardiac Remodeling through CtBP1-Associated repression of Nr4a1.iScience · 2026Article
- Decoding common and rare noncoding variant effects across cellular and developmental contexts.Nature genetics · 2026Article
- Smooth Muscle Cell Cytoglobin is a Negative Regulator of Atherosclerotic Fibrous Cap Development.bioRxiv : the preprint server for biology · 2026Article
- Atherosclerosis Profiling Reveals BHLHE40 as a Candidate Modulator of VSMC.Circulation research · 2026Article
- Spatially-Resolved Multiomic Atlas of Leiomyosarcoma Identifies Two Clinically Relevant Epigenetically-Driven Cell States.bioRxiv : the preprint server for biology · 2026Article
- Quantitative proteomics identifies clusterin as a novel biomarker for atherosclerosis.Animal models and experimental medicine · 2026Article
- Vascular smooth muscle cell state trajectories mediate molecular mechanisms of coronary disease risk.Nature communications · 2026Article
- Zinc finger proteins (ZFPs) in health and disease.Molecular biomedicine · 2026Review
- HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells.JACC. Basic to translational science · 2026Article
- Targeting modulated vascular smooth muscle cells in atherosclerosis via FAP-directed immunotherapy.Science (New York, N.Y.) · 2026Article
- Review
- Decoding Vascular Cell Diversity: Single-Cell Approaches to Mechanisms of Vascular Disease.Circulation research · 2026Review
- Functional Genomics Link REST to Endothelial Plasticity and Atherosclerosis.Circulation research · 2026Article
- Transcription factor ZEB2 is essential for ureteral smooth muscle cell differentiation.PLoS genetics · 2026Article
- A cell and transcriptome atlas of human arterial vasculature.Cell genomics · 2025Article
- Epigenomic landscape of single vascular cells reflects developmental origin and disease risk loci.Molecular systems biology · 2025Article
- Macrophage-like smooth muscle cells in atherosclerosis.Molecular biology reports · 2025Review
- Smooth muscle expression of RNA editing enzyme ADAR1 controls activation of the RNA sensor MDA5 in atherosclerosis.Nature cardiovascular research · 2025Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSmooth muscle cells (SMCs) transition into a number of different phenotypes during atherosclerosis, including those that resemble fibroblasts and chondrocytes, and make up the majority of cells in the atherosclerotic plaque. To better understand the epigenetic and transcriptional mechanisms that mediate these cell state changes, and how they relate to risk for coronary artery disease (CAD), we have investigated the causality and function of transcription factors at genome-wide associated loci.
methodsWe used CRISPR-Cas 9 genome and epigenome editing to identify the causal gene and cells for a complex CAD genome-wide association study signal at 2q22.3. Single-cell epigenetic and transcriptomic profiling in murine models and human coronary artery smooth muscle cells were used to understand the cellular and molecular mechanism by which this CAD risk gene exerts its function.
resultsCRISPR-Cas 9 genome and epigenome editing showed that the complex CAD genetic signals within a genomic region at 2q22.3 lie within smooth muscle long-distance enhancers for
conclusionsThese studies identify
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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.