Macrophage phenotypes in atherosclerosis

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 he...

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Bibliographic Details
Published in:Immunological reviews 2014-11, Vol.262 (1), p.153-166
Main Authors: Colin, Sophie, Chinetti-Gbaguidi, Giulia, Staels, Bart
Format: Article
Language:English
Subjects:
Animals
atherosclerosis
Atherosclerosis - etiology
Atherosclerosis - pathology
Cell Movement
chemokines
cytokines
Humans
inflammation
lipids
Macrophage Activation
macrophages
Macrophages - immunology
Macrophages - metabolism
Phenotype
Plaque, Atherosclerotic - immunology
Plaque, Atherosclerotic - metabolism
Plaque, Atherosclerotic - pathology
polarization
Transcription Factors - metabolism
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Summary: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.
ISSN:0105-2896
1600-065X
DOI:10.1111/imr.12218