ReviewThe Journal of clinical investigation2022
Through the layers: how macrophages drive atherosclerosis across the vessel wall.
Review in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 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
61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Gut microbiota regulate atherosclerosis via the gut-vascular axis: a scoping review of mechanisms and therapeutic interventions.Frontiers in microbiology · 2025Pooled it
- Subclinical atherosclerosis in Behcet's disease and its inverse relation to azathioprine use: an updated meta-analysis.Clinical and experimental medicine · 2023Pooled it
- Ilexoside K Ameliorates Atherosclerosis by Suppressing CD72Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- S100A8/A9 and S100A12 Proteins and Macrophage Polarization: Therapeutic Targets in Atherosclerosis.Biomolecules · 2026Review
- Ferroptosis in Vascular Diseases: A Mechanistic and Immunological Perspective on Therapeutic Targeting.Antioxidants (Basel, Switzerland) · 2026Review
- Endothelial NEDD4L exacerbates acute lung injury by targeting A20 for ubiquitination degradation.Respiratory research · 2026Article
- The Role of Glutathione Peroxidase 4 in Atherosclerosis: Role and Therapeutic Potential.Reviews in cardiovascular medicine · 2026Review
- Dysregulated Sheddase Signalling as a Molecular Driver of Plaque Instability Revealed by Integrative Transcriptomics.Journal of cellular and molecular medicine · 2026Article
- Interleukin-18 Inhibition Aggravates Atherosclerosis in Jak2JACC. Basic to translational science · 2026Article
- Delving into pyroptosis in atherosclerosis: role, mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity.Frontiers in immunology · 2026Review
- Ferroptosis in arterial atherosclerosis: mechanistic hypotheses, cell type specific vulnerabilities, translational biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Loss of immunometabolic adaptability in MASH: gut-derived signals drive macrophage reprogramming and fibrosis.Frontiers in immunology · 2026Review
- Maresin 1 Ameliorates Diabetic Kidney Disease in Mice by Promoting Macrophage M2 Polarization.Mediators of inflammation · 2026Article
- Cross-talk between lipopolysaccharide tolerance and AGEs in the regulation of macrophage inflammation and cholesterol efflux.Frontiers in immunology · 2026Article
- Foam Cells: The Origin of Formation and Target for Plant-derived Bioactive Compounds.Current medicinal chemistry · 2026Review
- The dual role of metabolic reprogramming in macrophage polarization in rheumatoid arthritis and coronary heart disease and the intervention strategy of traditional Chinese medicine.Frontiers in cardiovascular medicine · 2026Review
- Sphingolipid Metabolism: A Pathological Hub Linking Lipid Dysregulation and Chronic Inflammation in Atherosclerotic Cardiovascular Disease.Journal of inflammation research · 2026Review
- Article
- Regulation of lipoprotein processing by GPNMB in foamy macrophages: potential therapeutic targets for atherosclerosis.Nature communications · 2025Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiovascular disease (CVD) accounts for almost half of all deaths related to non-communicable disease worldwide, making it the single largest global cause of mortality. Although the risk factors for coronary artery disease - the most common cause of CVD - are well known and include hypertension, high cholesterol, age, and genetics, CVDs are now recognized as chronic inflammatory conditions. Arterial blockages, known as atherosclerosis, develop due to excess cholesterol accumulating within the arterial wall, creating a perpetually inflammatory state. The normally quiescent intimal layer of the vessel wall becomes laden with inflammatory cells, which alters the surrounding endothelial, smooth muscle, and extracellular matrix components to propagate disease. Macrophages, which can be either tissue resident or monocyte derived, are a key player in atherosclerotic disease progression and regression, and the understanding of their functions and origins continues to evolve with the use of deep phenotyping methodologies. This Review outlines how macrophages interact with each layer of the developing atherosclerotic plaque and discusses new concepts that are challenging our previous views on how macrophages function and our evolving understanding of the contribution of macrophages to disease.
Indexed as
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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.