ArticleJournal of lipid research2010
Arterial colony stimulating factor-1 influences atherosclerotic lesions by regulating monocyte migration and apoptosis.
Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 61 citations in OpenAlex.
- Single-Cell Multimodal Profiling Reveals a Novel CD26Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Aldosterone-Induced Transformation of Vascular Smooth Muscle Cells into Macrophage-like Cells Participates in Inflammatory Vascular Lesions.International journal of molecular sciences · 2025Article
- Effect of colony‑stimulating factor in the mechanism of bone metastasis development (Review).Oncology reports · 2024Review
- In Vitro Anti-Inflammatory and Vasculoprotective Effects of Red Cell Extract from the Black Sea UrchinNutrients · 2023Article
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- Identification and validation of hub genes involved in foam cell formation and atherosclerosis developmentPeerJ · 2023Article
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- Exploring the "gene-protein-metabolite" network of coronary heart disease with phlegm and blood stasis syndrome by integrated multi-omics strategy.Frontiers in pharmacology · 2022Article
- Natural Compound Resveratrol Attenuates TNF-Alpha-Induced Vascular Dysfunction in Mice and Human Endothelial Cells: The Involvement of the NF-κB Signaling Pathway.International journal of molecular sciences · 2021Article
- Metabolic regulation of macrophage proliferation and function in atherosclerosis.Current opinion in lipidology · 2021Review
- Treatment With the CSF1R Antagonist GW2580, Sensitizes Microglia to Reactive Oxygen Species.Frontiers in immunology · 2021Article
- Local M-CSF (Macrophage Colony-Stimulating Factor) Expression Regulates Macrophage Proliferation and Apoptosis in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Apoptosis of hematopoietic progenitor-derived adipose tissue-resident macrophages contributes to insulin resistance after myocardial infarction.Science translational medicine · 2020Article
- Sex as a Biological Variable in Atherosclerosis.Circulation research · 2020Review
- Distinct macrophage phenotypes skewed by local granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) are associated with tissue destruction and intimal hyperplasia in giant cell arteritis.Clinical & translational immunology · 2020Article
- Engineering Immunomodulatory Biomaterials for Regenerating the Infarcted Myocardium.Frontiers in bioengineering and biotechnology · 2020Article
- Transcriptional Activation of Matricellular Protein Spondin2 (SPON2) by BRG1 in Vascular Endothelial Cells Promotes Macrophage Chemotaxis.Frontiers in cell and developmental biology · 2020Article
- Growth Factors as Immunotherapeutic Targets in Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- Olive Leaf Extract Attenuates Inflammatory Activation and DNA Damage in Human Arterial Endothelial Cells.Frontiers in cardiovascular medicine · 2019Article
- Macrophage Depletion in Elderly Mice Improves Response to Tumor Immunotherapy, Increases Anti-tumor T Cell Activity and Reduces Treatment-Induced Cachexia.Frontiers in genetics · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have shown that colony stimulating factor-1 (CSF-1) deficiency dramatically reduced atherogenesis in mice. In this report we investigate this mechanism and explore a therapeutic avenue based on inhibition of CSF-1 signaling. Lesions from macrophage colony stimulating factor-1 (Csf1)+/- mice showed increased numbers of apoptotic macrophages, decreased overall macrophage content, and inflammation. In vitro studies indicated that CSF-1 is chemotactic for monocytes. Bone marrow transplantation studies suggested that vascular cell-derived, rather than macrophage-derived, CSF-1 is responsible for the effect on atherosclerosis. Consistent with previous studies, CSF-1 affected lesion development in a dose-dependent manner, suggesting that pharmacological inhibition of CSF-1 might achieve similar results. Indeed, we observed that treatment of hyperlipidemic mice with a CSF-1 receptor kinase inhibitor inhibited plaque progression. This observation was accompanied by a reduction in the expression of adhesion factors (ICAM-1), macrophage markers (F4/80), inflammatory cytokines (Il-6, Il-1beta), and macrophage matrix degradation enzymes (MMP-9). We conclude that the M-CSF pathway contributes to monocyte recruitment and macrophage survival and that this pathway is a potential target for therapeutic intervention.
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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.