ArticleNature medicine2013
Local proliferation dominates lesional macrophage accumulation in atherosclerosis.
Article in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 561 papers.
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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
561 citing papers in PubMed.
- RNA-Binding Proteins Regulate Cardiovascular Disease Progression Through Alternative Splicing and Alternative Polyadenylation.Journal of cardiovascular translational research · 2026Review
- Rare-Earth Nanomaterials for Advanced Theranostics of Atherosclerosis.Chemical & biomedical imaging · 2026Review
- Nucleic Acids as Emerging Regulators of Calcium Phosphate Biomineralization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Endoluminal Catheter Pulsed Field Ablation for the Treatment of Atherosclerotic Vascular Disease.Annals of biomedical engineering · 2026Article
- Macrophage CCRL2 promotes NLRP3 inflammasome activation to exacerbate atherosclerosis.Cellular & molecular immunology · 2026Article
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Carotid plaque macrophage burden and inflammatory lipid-associated macrophage markers predict secondary major adverse cardiovascular events after endarterectomy.European heart journal · 2026Article
- Pulmonary mRNA-LNP vaccines for rapid and durable protection against bacterial infection.Nature communications · 2026Article
- Emerging biomedical and pharmaceutical strategies for the treatment of atherosclerosis: from conventional lipid-lowering therapy to nanomedicine.Journal of applied biomedicine · 2026Review
- Mechanisms and therapeutic potential of colchicine in atherosclerotic cardiovascular disease.Nature cardiovascular research · 2026Review
- Temporal remodeling of atherosclerotic lipoprotein profiles and inflammatory markers after percutaneous coronary intervention: a real-world longitudinal study.BMC cardiovascular disorders · 2026Article
- CD47 Blockade Reprograms the Monocyte-Macrophage Axis to Promote Inflammation Resolution in Atherosclerosis.bioRxiv : the preprint server for biology · 2026Article
- A Mathematical Model for Smooth Muscle Cell Phenotype Switching In Atherosclerotic Plaque.Bulletin of mathematical biology · 2026Article
- The Role of Glutathione Peroxidase 4 in Atherosclerosis: Role and Therapeutic Potential.Reviews in cardiovascular medicine · 2026Review
- Influenza hijacks myeloid cells to inflict type-I interferon-fueled damage in the heart.Immunity · 2026Article
- Aggressive cholesterol lowering normalizes atherosclerosis regression in Jak2Journal of lipid research · 2026Article
- HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells.JACC. Basic to translational science · 2026Article
- TGFBI promotes liver fibrosis through remodeling the profibrotic microenvironment by a positive feedback regulatory loop.Communications biology · 2026Article
- Environmental modulators of vascular physiology and inflammation.Experimental physiology · 2026Review
- A Road Map to Understanding Cardiovascular Disease in Diabetes: From the AHA Strategically Focused Research Network in Cardiometabolic Health and Type 2 Diabetes.Circulation research · 2026Review
501 more citing papers are in PubMed but not listed here.
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20 authors.
Funding
Abstract
During the inflammatory response that drives atherogenesis, macrophages accumulate progressively in the expanding arterial wall. The observation that circulating monocytes give rise to lesional macrophages has reinforced the concept that monocyte infiltration dictates macrophage buildup. Recent work has indicated, however, that macrophage accumulation does not depend on monocyte recruitment in some inflammatory contexts. We therefore revisited the mechanism underlying macrophage accumulation in atherosclerosis. In murine atherosclerotic lesions, we found that macrophages turn over rapidly, after 4 weeks. Replenishment of macrophages in these experimental atheromata depends predominantly on local macrophage proliferation rather than monocyte influx. The microenvironment orchestrates macrophage proliferation through the involvement of scavenger receptor A (SR-A). Our study reveals macrophage proliferation as a key event in atherosclerosis and identifies macrophage self-renewal as a therapeutic target for cardiovascular disease.
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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.