Macrophages heterogeneity in atherosclerosis: implications for therapy

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Atherosclerosis is a chronic inflammatory disease occurring within the artery wall and is an underlying cause of cardiovascular complications, including myocardial infarction, stroke and peripheral vascular disease. Its pathogenesis involves many immune cell types with a well accepted role for monocyte/macrophages. Cholesterol-loaded macrophages are a characteristic feature of plaques and are major players in all stages of plaque development. As well as modulating lipid metabolism, macrophages secrete inflammatory cytokines, chemokines and reactive oxygen and nitrogen species that drive pathogenesis. They also produce proteases and tissue factor that contribute to plaque rupture and thrombosis. Macrophages are however heterogeneous cells and when appropriately activated, they phagocytose cytotoxic lipoproteins, clear apoptotic bodies, secrete anti-inflammatory cytokines and synthesize matrix repair proteins that stabilize vulnerable plaques. Pharmacological modulation of macrophage activity therefore represents a potential therapeutic strategy for atherosclerosis. The aim of this review is to provide an overview of the current understanding of the different macrophage subsets and their monocyte precursors, and, the implications of these subsets for atherosclerosis. This will present a foundation for highlighting novel opportunities to exploit the heterogeneity of macrophages as important diagnostic and therapeutic targets for atherosclerosis and its associated diseases.
Original languageEnglish
Pages (from-to)2055-2065
Number of pages11
JournalJournal of Cellular and Molecular Medicine
Volume14
Issue number8
Early online date12 Jul 2010
DOIs
Publication statusPublished - Aug 2010

Fingerprint

Atherosclerosis
Macrophages
Therapeutics
Monocytes
Cytokines
Reactive Nitrogen Species
Peripheral Vascular Diseases
Thromboplastin
Lipid Metabolism
Phagocytosis
Chemokines
Lipoproteins
Rupture
Reactive Oxygen Species
Thrombosis
Peptide Hydrolases
Chronic Disease
Anti-Inflammatory Agents
Arteries
Stroke

Keywords

  • monocyte
  • macrophage
  • M1
  • M2
  • activation
  • atherosclerosis
  • inflammation
  • immunomodulation
  • imaging
  • plaque stability

Cite this

Macrophages heterogeneity in atherosclerosis : implications for therapy. / Wilson, Heather M.

In: Journal of Cellular and Molecular Medicine, Vol. 14, No. 8, 08.2010, p. 2055-2065.

Research output: Contribution to journalArticle

@article{ecc182d712c54cdc94c534646e776a21,
title = "Macrophages heterogeneity in atherosclerosis: implications for therapy",
abstract = "Atherosclerosis is a chronic inflammatory disease occurring within the artery wall and is an underlying cause of cardiovascular complications, including myocardial infarction, stroke and peripheral vascular disease. Its pathogenesis involves many immune cell types with a well accepted role for monocyte/macrophages. Cholesterol-loaded macrophages are a characteristic feature of plaques and are major players in all stages of plaque development. As well as modulating lipid metabolism, macrophages secrete inflammatory cytokines, chemokines and reactive oxygen and nitrogen species that drive pathogenesis. They also produce proteases and tissue factor that contribute to plaque rupture and thrombosis. Macrophages are however heterogeneous cells and when appropriately activated, they phagocytose cytotoxic lipoproteins, clear apoptotic bodies, secrete anti-inflammatory cytokines and synthesize matrix repair proteins that stabilize vulnerable plaques. Pharmacological modulation of macrophage activity therefore represents a potential therapeutic strategy for atherosclerosis. The aim of this review is to provide an overview of the current understanding of the different macrophage subsets and their monocyte precursors, and, the implications of these subsets for atherosclerosis. This will present a foundation for highlighting novel opportunities to exploit the heterogeneity of macrophages as important diagnostic and therapeutic targets for atherosclerosis and its associated diseases.",
keywords = "monocyte, macrophage, M1, M2, activation, atherosclerosis, inflammation, immunomodulation, imaging, plaque stability",
author = "Wilson, {Heather M}",
year = "2010",
month = "8",
doi = "10.1111/j.1582-4934.2010.01121.x",
language = "English",
volume = "14",
pages = "2055--2065",
journal = "Journal of Cellular and Molecular Medicine",
issn = "1582-1838",
publisher = "Wiley-Blackwell",
number = "8",

}

TY - JOUR

T1 - Macrophages heterogeneity in atherosclerosis

T2 - implications for therapy

AU - Wilson, Heather M

PY - 2010/8

Y1 - 2010/8

N2 - Atherosclerosis is a chronic inflammatory disease occurring within the artery wall and is an underlying cause of cardiovascular complications, including myocardial infarction, stroke and peripheral vascular disease. Its pathogenesis involves many immune cell types with a well accepted role for monocyte/macrophages. Cholesterol-loaded macrophages are a characteristic feature of plaques and are major players in all stages of plaque development. As well as modulating lipid metabolism, macrophages secrete inflammatory cytokines, chemokines and reactive oxygen and nitrogen species that drive pathogenesis. They also produce proteases and tissue factor that contribute to plaque rupture and thrombosis. Macrophages are however heterogeneous cells and when appropriately activated, they phagocytose cytotoxic lipoproteins, clear apoptotic bodies, secrete anti-inflammatory cytokines and synthesize matrix repair proteins that stabilize vulnerable plaques. Pharmacological modulation of macrophage activity therefore represents a potential therapeutic strategy for atherosclerosis. The aim of this review is to provide an overview of the current understanding of the different macrophage subsets and their monocyte precursors, and, the implications of these subsets for atherosclerosis. This will present a foundation for highlighting novel opportunities to exploit the heterogeneity of macrophages as important diagnostic and therapeutic targets for atherosclerosis and its associated diseases.

AB - Atherosclerosis is a chronic inflammatory disease occurring within the artery wall and is an underlying cause of cardiovascular complications, including myocardial infarction, stroke and peripheral vascular disease. Its pathogenesis involves many immune cell types with a well accepted role for monocyte/macrophages. Cholesterol-loaded macrophages are a characteristic feature of plaques and are major players in all stages of plaque development. As well as modulating lipid metabolism, macrophages secrete inflammatory cytokines, chemokines and reactive oxygen and nitrogen species that drive pathogenesis. They also produce proteases and tissue factor that contribute to plaque rupture and thrombosis. Macrophages are however heterogeneous cells and when appropriately activated, they phagocytose cytotoxic lipoproteins, clear apoptotic bodies, secrete anti-inflammatory cytokines and synthesize matrix repair proteins that stabilize vulnerable plaques. Pharmacological modulation of macrophage activity therefore represents a potential therapeutic strategy for atherosclerosis. The aim of this review is to provide an overview of the current understanding of the different macrophage subsets and their monocyte precursors, and, the implications of these subsets for atherosclerosis. This will present a foundation for highlighting novel opportunities to exploit the heterogeneity of macrophages as important diagnostic and therapeutic targets for atherosclerosis and its associated diseases.

KW - monocyte

KW - macrophage

KW - M1

KW - M2

KW - activation

KW - atherosclerosis

KW - inflammation

KW - immunomodulation

KW - imaging

KW - plaque stability

U2 - 10.1111/j.1582-4934.2010.01121.x

DO - 10.1111/j.1582-4934.2010.01121.x

M3 - Article

VL - 14

SP - 2055

EP - 2065

JO - Journal of Cellular and Molecular Medicine

JF - Journal of Cellular and Molecular Medicine

SN - 1582-1838

IS - 8

ER -