Role of colony-stimulating factors in atherosclerosis
Abstract
PURPOSE OF REVIEW: The varied effects of colony-stimulating factors (CSFs) on monocytes and macrophages during inflammation and atherosclerosis and its clinical presentation prompt the question whether the differing effects of CSFs dictate macrophage function and disease progression. RECENT FINDINGS: CSFs can give rise to heterogeneous populations of monocyte-derived macrophages that are characterized by disparate expression of distinct molecules which dictate their ability to process lipid and regulate inflammatory and immune responses. The CSFs have been found within atherosclerotic plaques and in the circulation where their levels may act as predictive biomarkers of disease progression. Accordingly, differing exposure to these factors imparts divergent genomic signatures and functional properties on macrophages and may impact the multifactorial steps involved in atherogenesis, plaque progression and instability. SUMMARY: Great interest in macrophage heterogeneity in the genesis and progression of atherosclerosis has led to the search for consistent markers of specific subsets in both animal models and humans. A better understanding of the overlap and competition between CSF regulation of macrophage phenotypes is therefore warranted, to allow their characterization in plaques. Subsequent targeted genetic and pharmacological intervention will facilitate the generation of therapeutic approaches to halt the progression and rupture of advanced atherosclerotic plaques.
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GM-CSF and M-CSF are widely expressed in the vascular wall and regulate monocyte-to-macrophage differentiation as well as mature macrophage number and function.
“Two colony-stimulating factors, granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF), are widely expressed in the vascular wall149.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [149]
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Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities
Bäck, M., Yurdagul, A., Tabas, I., Öörni, K., & Kovanen, P. T. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0169-2 · Cited by 1,341 · see citing works
Schiopu, A., Bengtsson, E., Gonçalves, I., Nilsson, J., Fredrikson, G. N., & Björkbacka, H. (2016) · Journal of the American Heart Association · doi:10.1161/jaha.115.002851 · Cited by 25 · see citing works
- Authors
- Di Gregoli, K., & Johnson, J. L.
- Affiliations
- Bristol Royal Infirmary (GB)
- Corresponding author
- Johnson, Jason L.
- ORCID
- Johnson, Jason L.
- Venue
- Current Opinion in Lipidology
- Published
- 2012-10
- Volume
- 23
- Issue
- 5
- Pages
- 412-421
- ISSN
- 0957-9672 (ISSN-L)
- OpenAlex
- W2017082716
- Cited by
- 55
- References
- 66
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 1 · 2023: 5 · 2022: 5 · 2021: 2 · 2020: 4 · 2019: 2 · 2018: 1 · 2017: 6 · 2016: 8 · 2015: 7 · 2014: 5 · 2013: 3
- FWCI
- 0.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Lipidology (publishedVersion)
- PubMed (publishedVersion)
- Explore Bristol Research (submittedVersion)
- Funders
- British Heart Foundation (FS/07/053/24069)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- colony-stimulating factors, atherosclerosis, macrophage heterogeneity, monocyte-derived macrophages, atherosclerotic plaque, macrophage polarization, lipid processing, inflammation, disease progression biomarkers, plaque vulnerability, atherogenesis
- MeSH terms
- Animals, Humans, Immunologic Factors, Inflammation, Macrophages, Monocytes, Phenotype, Biomarkers, Macrophage Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, Cell Polarity, Disease Progression, Atherosclerosis, Matrix Metalloproteinase 14, Plaque, Atherosclerotic
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