Macrophage phenotypes in atherosclerosis
Abstract
Summary: Initiation and progression of atherosclerosis depend on local inflammation and accumulation of lipids in the vascular wall. Although many cells are involved in the development and progression of atherosclerosis, macrophages are fundamental contributors. For nearly a decade, the phenotypic heterogeneity and plasticity of macrophages has been studied. In atherosclerotic lesions, macrophages are submitted to a large variety of micro‐environmental signals, such as oxidized lipids and cytokines, which influence the phenotypic polarization and activation of macrophages resulting in a dynamic plasticity. The macrophage phenotype spectrum is characterized, at the extremes, by the classical M1 macrophages induced by T‐helper 1 (Th‐1) cytokines and by the alternative M2 macrophages induced by Th‐2 cytokines. M2 macrophages can be further classified into M2a, M2b, M2c, and M2d subtypes. More recently, additional plaque‐specific macrophage phenotypes have been identified, termed as Mox, Mhem, and M4. Understanding the mechanisms and functional consequences of the phenotypic heterogeneity of macrophages will contribute to determine their potential role in lesion development and plaque stability. Furthermore, research on macrophage plasticity could lead to novel therapeutic approaches to counteract cardiovascular diseases such as atherosclerosis. The present review summarizes our current knowledge on macrophage subsets in atherosclerotic plaques and mechanism behind the modulation of the macrophage phenotype.
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Macrophages in cell culture and mice show high plasticity to adopt various phenotypes, as reflected in extended subgroup classifications.
“In both cell culture systems and experimental animals (such as mice), macrophages have a high degree of plasticity to adopt various phenotypes, exemplified by the extended classification of the macrophages into a number of subgroups153.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [153]
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- Authors
- Colin, S., Chinetti‐Gbaguidi, G., & Staels, B.
- Affiliations
- Inserm (FR)
- Université Lille 2 Lille France
- Corresponding author
- Staels, Bart
- ORCID
- Staels, Bart
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2014-10-15
- Volume
- 262
- Issue
- 1
- Pages
- 153-166
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2085069678
- Cited by
- 657
- References
- 165
- Citations by year
- 2026: 33 · 2025: 51 · 2024: 95 · 2023: 79 · 2022: 78 · 2021: 61 · 2020: 59 · 2019: 53 · 2018: 37 · 2017: 38 · 2016: 35 · 2015: 33 · 2014: 4
- FWCI
- 3.58
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Institut Universitaire de France
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- atherosclerosis, macrophage phenotype, macrophage plasticity, M1 macrophages, M2 macrophages, Th1 cytokines, Th2 cytokines, oxidized lipids, plaque stability, atherosclerotic plaque, macrophage polarization
- MeSH terms
- Animals, Cell Movement, Humans, Macrophage Activation, Macrophages, Phenotype, Transcription Factors, Atherosclerosis, Plaque, Atherosclerotic
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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