Mechanisms and consequences of efferocytosis in advanced atherosclerosis
Open accessAbstract
Review on how dangerous atherosclerotic plaques form and the critical role for defective phagocytic clearance (or “efferocytosis”) of apoptotic macrophages in these lesions. Throughout atherosclerotic lesion development, intimal macrophages undergo apoptosis, a form of death that usually prevents cellular necrosis. In advanced atherosclerotic lesions, however, these apoptotic macrophages become secondarily necrotic and coalesce over time into a key feature of vulnerable plaques, the necrotic core. This event is critically important, as necrotic core formation in these advanced atheromata is thought to promote plaque disruption and ultimately, acute atherothrombotic vascular disease. Increasing evidence suggests that the mechanism behind postapoptotic macrophage necrosis in advanced atherosclerosis is defective phagocytic clearance or “efferocytosis” of the apoptotic cells. Thus, understanding the cellular and molecular mechanisms of efferocytosis in atherosclerosis and why efferocytosis becomes defective in advanced lesions is an important goal. Molecular–genetic causation studies in mouse models of advanced atherosclerosis have provided evidence that several molecules known to be involved in efferocytosis, including TG2, MFG-E8, complement C1q, Mertk, lysoPC, and Fas, play important roles in the clearance of apoptotic cells in advanced plaques. These and future insights into the molecular mechanisms of defective efferocytosis in advanced atheromata may open the way for novel therapeutic strategies for atherothrombotic vascular disease, the leading cause of death in the industrialized world.
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Failure to clear dead cells in atherosclerotic lesions causes accumulation of secondarily necrotic cells and formation of a highly inflammatory necrotic core.
“Failure to clear dead cells in the atherosclerotic lesion leads to the accumulation of secondarily necrotic cells and the formation of a highly inflammatory necrotic core188,189.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [188]
Defective efferocytosis has a particularly prominent role in atherosclerosis.
“The inability to clear apoptotic cells efficiently drives many diseases, but defective effero-cytosis has a particularly prominent role in atheroscle-rosis188–190.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [188]
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Brophy, M. L., Dong, Y., Wu, H., Rahman, H. N. A., Song, K., & Chen, H. (2017) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2017.00002 · Cited by 68 · see citing works
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Bruns, H., & Stenger, S. (2014) · Future Microbiology · doi:10.2217/fmb.13.164 · Cited by 47 · see citing works
Efferocytosis Creates a Tumor Microenvironment Supportive of Tumor Survival and Metastasis
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- Authors
- Thorp, E., & Tabas, I.
- Affiliations
- Columbia University Irving Medical Center (US)
- Corresponding author
- Tabas, Ira
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-05-04
- Volume
- 86
- Issue
- 5
- Pages
- 1089-1095
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- PMC
- PMC2774877
- OpenAlex
- W2130035132
- Cited by
- 231
- References
- 71
- Citations by year
- 2026: 15 · 2025: 9 · 2024: 8 · 2023: 9 · 2022: 13 · 2021: 7 · 2020: 11 · 2019: 13 · 2018: 11 · 2017: 13 · 2016: 18 · 2015: 25 · 2014: 24 · 2013: 18 · 2012: 14
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (HL54591, HL75662)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- efferocytosis, advanced atherosclerosis, macrophage apoptosis, necrotic core, vulnerable plaque, plaque rupture, phagocytic clearance, tissue transglutaminase, MFG-E8, C1q, MERTK, lysophosphatidylcholine, Fas, mouse model
- MeSH terms
- Animals, Brain, Cerebral Arteries, Disease Models, Animal, Humans, Macrophages, Necrosis, Phagocytosis, Apoptosis, Atherosclerosis, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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