Macrophages in the Pathogenesis of Atherosclerosis
Open accessAbstract
In atherosclerosis, the accumulation of apolipoprotein B-lipoproteins in the matrix beneath the endothelial cell layer of blood vessels leads to the recruitment of monocytes, the cells of the immune system that give rise to macrophages and dendritic cells. Macrophages derived from these recruited monocytes participate in a maladaptive, nonresolving inflammatory response that expands the subendothelial layer due to the accumulation of cells, lipid, and matrix. Some lesions subsequently form a necrotic core, triggering acute thrombotic vascular disease, including myocardial infarction, stroke, and sudden cardiac death. This Review discusses the central roles of macrophages in each of these stages of disease pathogenesis.
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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 [46]
Atherosclerosis etiology includes inflammatory cells, particularly macrophages.
“Similar to cancer, atherosclerosis has an etiology that has, for many years, been recognized to include the involvement an inflammatory cell population, in particular macrophages [45–47].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [46]
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Site-Specific Effects of PECAM-1 on Atherosclerosis in LDL Receptor–Deficient Mice
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Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia
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Imaging Atherosclerosis and Vulnerable Plaque
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A Macrophage Sterol-Responsive Network Linked to Atherogenesis
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Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis
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Defective cholesterol clearance limits remyelination in the aged central nervous system
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Tumour‐associated macrophages act as a slow‐release reservoir of nano‐therapeutic Pt(IV) pro‐drug
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High-protein diets increase cardiovascular risk by activating macrophage mTOR to suppress mitophagy
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Self-citationMacrophages retain hematopoietic stem cells in the spleen via VCAM-1
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“This process may be similar to how macrophages contribute to atherosclerotic plaques when failure to efficiently eliminate lipids results in the formation of foam cells in cardiovascular disease (Moore and Tabas, 2011).”
BackgroundEfferocytosis in atherosclerotic lesions: Malfunctioning regulatory pathways and control mechanisms
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“While defective removal of dead phagocytes is assumed to be detrimental in other conditions such as atherosclerosis (Moore & Tabas, 2011), its reasons and significance in this disease await further clarification.”
BackgroundLineage tracing of cells involved in atherosclerosis
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“, vitronectin, complement factors, and apolipoprotein E) and important amounts of cholesterol and cholesterol esters (Moore and Tabas 2011; Pikuleva and Curcio 2014; Hageman and Mullins 1999; Mullins et al. 2000; Curcio et al. 2001).”
BackgroundInfluentialMonocytes and macrophages as protagonists in vascular complications of diabetes
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The macrophage LBP gene is an LXR target that promotes macrophage survival and atherosclerosis
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Rational design of lipid-activatable NIR-II probes for precisely imaging atherosclerotic plaque
Xu, X., Ma, Y., Cao, H., Xu, L., Chen, H., Liu, S., Sun, W., Song, G., & Zhang, X.-B. (2025) · Science China Chemistry · doi:10.1007/s11426-024-2361-x · Cited by 21 · see citing works
Kaneko, C., Nitta, N., Tsuchiya, K., Watanabe, S., Nitta-Seko, A., Ohta, S., Otani, H., Sonoda, A., Murata, K., & Shiomi, M. (2015) · The British Journal of Radiology · doi:10.1259/bjr.20150167 · Cited by 11 · see citing works
- Authors
- Moore, K. J., & Tabas, I.
- Affiliations
- NYU Langone Health (US)
- Columbia University Irving Medical Center (US)
- Corresponding author
- Tabas, Ira
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 145
- Issue
- 3
- Pages
- 341-355
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3111065
- OpenAlex
- W2113934014
- Cited by
- 2,669
- References
- 104
- Citations by year
- 2026: 131 · 2025: 151 · 2024: 169 · 2023: 193 · 2022: 196 · 2021: 228 · 2020: 182 · 2019: 195 · 2018: 189 · 2017: 168 · 2016: 177 · 2015: 178 · 2014: 186 · 2013: 166 · 2012: 121
- FWCI
- 14.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 838 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG20255, R01AG020255)
- National Heart, Lung, and Blood Institute (P01HL054591, R01HL106019, R01HL057560, P01HL087123, R01HL075662)
- 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, monocyte recruitment, nonresolving inflammation, necrotic core, myocardial infarction, stroke, sudden cardiac death, dendritic cells
- MeSH terms
- Animals, Dendritic Cells, Humans, Macrophages, Monocytes, Signal Transduction, Atherosclerosis
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