ArticleAging2018
Integrated DNA methylation and gene expression analysis identifies SLAMF7 as a key regulator of atherosclerosis.
Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- DNA methylation and cardiovascular disease in humans: a systematic review and database of known CpG methylation sites.Clinical epigenetics · 2023Pooled it
- Novel DNA methylation signatures of tobacco smoking with trans-ethnic effects.Clinical epigenetics · 2021Pooled it
- Integrating untargeted metabolomics and deep learning approaches to identify specific metabolic signatures and new mechanisms in unstable plaques.Frontiers in cardiovascular medicine · 2026Article
- SLAMF7 and SLAMF8 receptors shape human plasmacytoid dendritic cell responses to intracellular bacteria.The Journal of clinical investigation · 2025Article
- SLAMF7 Promotes Foam Cell Formation of Macrophage by Suppressing NR4A1 Expression During Carotid Atherosclerosis.Inflammation · 2024Article
- DNA methylation and histone post-translational modifications in atherosclerosis and a novel perspective for epigenetic therapy.Cell communication and signaling : CCS · 2023Review
- Inhibition of pro-inflammatory signaling in human primary macrophages by enhancing arginase-2 via target site blockers.Molecular therapy. Nucleic acids · 2023Article
- Role of Macrophage lncRNAs in Mediating Inflammatory Processes in Atherosclerosis and Sepsis.Biomedicines · 2023Review
- Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease.Biomedicines · 2022Review
- SLAMF7 engagement superactivates macrophages in acute and chronic inflammation.Science immunology · 2022Article
- Hypomethylation of Rnase6 Promoter Enhances Proliferation and Migration of Murine Aortic Vascular Smooth Muscle Cells and Aggravates Atherosclerosis in Mice.Frontiers in bioengineering and biotechnology · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS) is a multifactorial disease. Exploration of DNA methylation in regulating gene transcription in a cell type- and stage-specific manner will shed light on understanding the biological processes associated with plaque stability. We identified 174 up-regulated genes with hypo-methylation in the promoter, and 86 down-regulated genes with hyper-methylation in the promoter, in AS vs. healthy controls. Among them, high expression of signaling lymphocytic activation molecule 7 (SLAM7) was examined in carotid plaque vs. intact tissue, in advanced plaque vs. early atherosclerotic tissue, and SLAMF7 protein expressed significantly higher in the unstable plaques than that in the stable plaques, especially in the CD68-positive macrophages. Depletion of SLAMF7 in plaque-derived macrophages induced a suppressed secretion of proinflammatory cytokines, and inhibited proliferation of vascular smooth muscle cells. These data provide emerging evidence that SLAMF7 could be a target of potential therapeutic intervention in carotid AS.
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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.