Monocytes in atherosclerosis: subsets and functions
Open accessAbstract
Chronic inflammation drives atherosclerosis, the leading cause of cardiovascular disease. Over the past two decades, data have emerged showing that immune cells are involved in the pathogenesis of atherosclerotic plaques. The accumulation and continued recruitment of leukocytes are associated with the development of 'vulnerable' plaques. These plaques are prone to rupture, leading to thrombosis, myocardial infarction or stroke, all of which are frequent causes of death. Plaque macrophages account for the majority of leukocytes in plaques, and are believed to differentiate from monocytes recruited from circulating blood. However, monocytes represent a heterogenous circulating population of cells. Experiments are needed to address whether monocyte recruitment to plaques and effector functions, such as the formation of foam cells, the production of nitric oxide and reactive oxygen species, and proteolysis are critical for the development and rupture of plaques, and thus for the pathophysiology of atherosclerosis, as well as elucidate the precise mechanisms involved.
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A macrophage phenotypic switch occurs with atherosclerosis progression.
“Also similar to cancer, a macrophage phenotypic switch is observed to occur with disease progression, albeit with significantly different pathologic sequelae [45–48].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [48]
Macrophages in atherosclerotic plaques account for the majority of leukocytes and inflammation and are implicated in plaque rupture, representing an important target.
“Macrophages in atherosclerotic plaques account for the majority of leukocytes and inflammation in plaques, and are implicated in plaque rupture, thereby representing an important target127.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [127]
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- Authors
- Woollard, K. J., & Geissmann, F.
- Affiliations
- King's College London (GB)
- Corresponding author
- Woollard, Kevin J.
- ORCID
- Woollard, Kevin J.
- Venue
- Nature Reviews Cardiology
- Published
- 2010-01-12
- Volume
- 7
- Issue
- 2
- Pages
- 77-86
- ISSN
- 1759-5002 (ISSN-L)
- 1759-5010
- PMC
- PMC2813241
- OpenAlex
- W1964369726
- Cited by
- 890
- References
- 92
- Citations by year
- 2026: 21 · 2025: 31 · 2024: 47 · 2023: 62 · 2022: 38 · 2021: 49 · 2020: 66 · 2019: 59 · 2018: 52 · 2017: 69 · 2016: 50 · 2015: 49 · 2014: 70 · 2013: 76 · 2012: 62
- FWCI
- 5.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Cardiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- British Heart Foundation (FS/09/003/26551)
- Versus Arthritis
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cerebrovascular and Carotid Artery Diseases
- Keywords
- monocytes, atherosclerosis, plaque macrophages, monocyte heterogeneity, monocyte recruitment, chronic inflammation, vulnerable plaque, plaque rupture, foam cells, nitric oxide, reactive oxygen species, proteolysis
- MeSH terms
- Animals, Cell Differentiation, Cell Movement, Humans, Inflammation, Macrophages, Monocytes, Rupture, Signal Transduction, Disease Progression, Inflammation Mediators, Atherosclerosis
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