ArticleThe Journal of clinical investigation2018
Alternative macrophages in atherosclerosis: not always protective!
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 55 citations in OpenAlex.
- Single-cell transcriptomics provides insights into the stress-immune interplay and informs disease risk.Cell genomics · 2026Article
- Cell apoptosis in ischemic stroke: Focus on lipid metabolism.Neural regeneration research · 2026Article
- Very low-density lipoprotein and the human health.World journal of experimental medicine · 2026Review
- Interplay Between KLF4, STAT, IRF, and NF-κB in VSMC and Macrophage Plasticity During Vascular Inflammation and Atherosclerosis.International journal of molecular sciences · 2025Review
- Identification and validation of core biomarkers for sepsis: a comprehensive analysis using bioinformatics and machine learning.Frontiers in immunology · 2025Article
- Targeting Macrophage Phenotypes and Metabolism as Novel Therapeutic Approaches in Atherosclerosis and Related Cardiovascular Diseases.Current atherosclerosis reports · 2024Review
- The Pathological Mechanisms and Therapeutic Molecular Targets in Arteriovenous Fistula Dysfunction.International journal of molecular sciences · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- The role of M1/M2 macrophage polarization in the pathogenesis of obesity-related kidney disease and related pathologies.Frontiers in immunology · 2024Review
- Macrophage polarization and metabolism in atherosclerosis.Cell death & disease · 2023Review
- Ironing out macrophages in atherosclerosis.Acta biochimica et biophysica Sinica · 2023Review
- Nature-inspired nanocarriers for improving drug therapy of atherosclerosis.Regenerative biomaterials · 2023Review
- Emerging Evidence of Pathological Roles of Very-Low-Density Lipoprotein (VLDL).International journal of molecular sciences · 2022Review
- AtheroSpectrum Reveals Novel Macrophage Foam Cell Gene Signatures Associated With Atherosclerotic Cardiovascular Disease Risk.Circulation · 2022Article
- Exosomes in atherosclerosis: Convergence on macrophages.International journal of biological sciences · 2022Review
- Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target.International journal of biological sciences · 2022Review
- Diverse Epigenetic Regulations of Macrophages in Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Foam Cells in Atherosclerosis: Novel Insights Into Its Origins, Consequences, and Molecular Mechanisms.Frontiers in cardiovascular medicine · 2022Review
- Differential Gene Expression and Immune Cell Infiltration in Carotid Intraplaque Hemorrhage Identified Using Integrated Bioinformatics Analysis.Frontiers in cardiovascular medicine · 2022Article
- Identification and Validation of Candidate Gene Module Along With Immune Cells Infiltration Patterns in Atherosclerosis Progression to Plaque RuptureFrontiers in cardiovascular medicine · 2022Article
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2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a chronic inflammatory disease of the vasculature that is initiated by cholesterol deposition into the arterial wall, which triggers the infiltration of immune and inflammatory cells, including monocytes and macrophages. As atherosclerotic plaques progress, localized hypoxia promotes compensatory angiogenesis from the vasa vasorum. Immature neovessels are prone to leakage, thus destabilizing the plaque and leading to intraplaque hemorrhage. Macrophages with different phenotypes, ranging from classical inflammatory subtypes to alternatively activated antiinflammatory macrophages, have been identified in atherosclerotic lesions. Antiinflammatory hemoglobin-scavenging CD163+ macrophages are present in neovessel- and hemorrhage-rich areas; however, the role of these macrophages in atherogenesis has been unclear. In this issue of the JCI, Guo, Akahori, and colleagues show that CD163+ macrophages promote angiogenesis, vessel permeability, and leucocyte infiltration in human and mouse atherosclerotic lesions through a mechanism involving hemoglobin:haptoglobin/CD163/HIF1α-mediated VEGF induction. This study thus identifies proatherogenic properties of CD163+ macrophages, which previously were thought to be beneficial.
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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.