ArticleCirculation research2022
The
Article in Circulation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 6 of them syntheses that pooled it.
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
35 citing papers in PubMed, 6 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- Genome and Transcriptome-Wide Analyses Identify Multiple Candidate Genes and a Significant Polygenic Contribution in Bicuspid Aortic Valve.Circulation · 2026Pooled it
- Macrophage-associated kinase signaling in atherosclerosis - a systematic review.Cell communication and signaling : CCS · 2026Pooled it
- Identification ofDepression and anxiety · 2025Pooled it
- Examining the potential causal relationships among smoking behaviors, blood DNA methylation profiles, and the development of coronary heart disease and myocardial infarction.Clinical epigenetics · 2024Pooled it
- Meta-analysis and transcriptomic analysis reveal that NKRF and ZBTB17 regulate the NF-κB signaling pathway, contributing to the shared molecular mechanisms of Alzheimer's disease and atherosclerosis.CNS neuroscience & therapeutics · 2024Pooled it
- Integrative genomic analyses identify candidate causal genes for calcific aortic valve stenosis involving tissue-specific regulation.Nature communications · 2024Pooled it
- Post‑translational modifications in atherosclerosis: Roles, mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2026Review
- Exploring the shared genetic architecture and causal relationship between childhood maltreatment and psychiatric disorders.Molecular psychiatry · 2026Article
- FHL3 Regulates Vascular Smooth Muscle Cell Phenotypic Switching Through the MRTFB-SRF Signaling Axis.Cells · 2026Article
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Integrative functional genomics analysis identifies pleiotropic genes for vascular diseases.Nature communications · 2026Article
- Identification of key biomarkers for myocardial infarction by multi-omics analysis and machine learning.Frontiers in immunology · 2026Article
- A single-cell and spatial atlas of plaque macrophage states in human atherosclerosis.Frontiers in immunology · 2026Review
- Epigenetic Mechanisms Linking Chronic Obstructive Pulmonary Disease and Atrial Fibrillation: A Multi-Omics Mendelian Randomization Study.International journal of chronic obstructive pulmonary disease · 2026Article
- Multi-omic underpinnings of heterogeneous aging across multiple organ systems.Cell genomics · 2025Article
- Gut microbiota-derived trimethylamine-N-oxide inhibits SIRT1 to regulate SM22α-mediated smooth muscle cell inflammation and promote atherosclerosis progression.Journal of cell communication and signaling · 2025Article
- The relationship between hemoglobin glycation index and the risk of cardiovascular disease in populations with diabetes or prediabetes: a population-based cohort study.Diabetology & metabolic syndrome · 2025Article
- Identification of plasma proteomic markers underlying polygenic risk of type 2 diabetes and related comorbidities.Nature communications · 2025Article
- CircBTBD7-420aa Encoded by hsa_circ_0000563 Regulates the Progression of Atherosclerosis and Construction of circBTBD7-420aa Engineered Exosomes.JACC. Basic to translational science · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 8 institutions in 6 countries.
Funding
Abstract
backgroundGenome-wide association studies have discovered a link between genetic variants on human chromosome 15q26.1 and increased coronary artery disease (CAD) susceptibility; however, the underlying pathobiological mechanism is unclear. This genetic locus contains the METHODS AND
resultsAnalyses of isogenic monocytic cell lines generated by CRISPR (clustered regularly interspaced short palindromic repeats)-mediated genome editing showed that monocytes with an engineered 15q26.1 CAD risk genotype had reduced FES expression. Small-interfering-RNA-mediated knockdown of FES promoted migration of monocytes and vascular smooth muscle cells. A phosphoproteomics analysis showed that FES knockdown altered phosphorylation of a number of proteins known to regulate cell migration. Single-cell RNA-sequencing revealed that in human atherosclerotic plaques, cells that expressed
conclusionsWe provide substantial evidence that the CAD risk variants at the 15q26.1 locus reduce FES expression in monocytes and that FES depletion results in larger atherosclerotic plaques with more monocytes/macrophages and smooth muscle cells. This study is the first demonstration that FES plays a protective role against atherosclerosis and suggests that enhancing FES activity could be a potentially novel therapeutic approach for CAD intervention.
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.