Macrophages in atherosclerosis: a dynamic balance
Open accessAbstract
Atherosclerosis is a chronic inflammatory disease that arises from an imbalance in lipid metabolism and a maladaptive immune response driven by the accumulation of cholesterol-laden macrophages in the artery wall. Through the analysis of the progression and regression of atherosclerosis in animal models, there is a growing understanding that the balance of macrophages in the plaque is dynamic and that both macrophage numbers and the inflammatory phenotype influence plaque fate. In this Review, we summarize recently identified pro- and anti-inflammatory pathways that link lipid and inflammation biology with the retention of macrophages in plaques, as well as factors that have the potential to promote their egress from these sites.
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Atherosclerosis is at least in part a disease of chronic inflammation, not unlike T2D.
“Therefore, atherosclerosis is at least in part a disease of chronic inflammation, not unlike T2D.”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Moore et al., 2013
Innate immune cells, particularly macrophages, have been implicated in vascular remodeling and atherosclerosis through production of reactive oxygen species and cytokines.
“In addition, innate immune cells, particularly macrophages, have been implicated in vascular remodeling and atherosclerosis through the production of ROS and cytokines (19).”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [19]
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- Authors
- Moore, K. J., Sheedy, F. J., & Fisher, E. A.
- Affiliations
- New York University (US)
- NYU Langone Health (US)
- Corresponding author
- Moore, Kathryn J.
- Fisher, Edward A.
- Venue
- Nature reviews. Immunology
- Published
- 2013-09-02
- Volume
- 13
- Issue
- 10
- Pages
- 709-721
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- PMC
- PMC4357520
- OpenAlex
- W2079724669
- Cited by
- 2,559
- References
- 117
- Citations by year
- 2026: 143 · 2025: 210 · 2024: 238 · 2023: 247 · 2022: 241 · 2021: 231 · 2020: 245 · 2019: 195 · 2018: 215 · 2017: 177 · 2016: 183 · 2015: 132 · 2014: 92 · 2013: 6
- FWCI
- 11.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG020255)
- National Heart, Lung, and Blood Institute (R01HL084312, R01HL117334, P01HL098055, R01 R01HL117334, R01HL108182)
- 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
- macrophages, atherosclerosis, atherosclerotic plaque, plaque regression, macrophage dynamics, lipid metabolism, inflammation, anti-inflammatory pathways, pro-inflammatory pathways, plaque stability
- MeSH terms
- Animals, Arteries, Cell Count, Cell Movement, Cholesterol, Humans, Inflammation, Macrophages, Monocytes, Biomarkers, Atherosclerosis, Lipid Metabolism, Mice, Plaque, Atherosclerotic
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