Macrophage death and defective inflammation resolution in atherosclerosis
Open accessAbstract
A key event in atherosclerosis is a maladaptive inflammatory response to subendothelial lipoproteins. A crucial aspect of this response is a failure to resolve inflammation, which normally involves the suppression of inflammatory cell influx, effective clearance of apoptotic cells and promotion of inflammatory cell egress. Defects in these processes promote the progression of atherosclerotic lesions into dangerous plaques, which can trigger atherothrombotic vascular disease, the leading cause of death in industrialized societies. In this Review I provide an overview of these concepts, with a focus on macrophage death and defective apoptotic cell clearance, and discuss new therapeutic strategies designed to boost inflammation resolution in atherosclerosis.
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Many chronic inflammatory diseases, including advanced atherosclerosis, are characterized by an imbalance between pro-resolving and pro-inflammatory mediators such as leukotrienes, leading to defective resolution, tissue injury, and DAMP-mediated inflammation.
“Many chronic inflammatory diseases, including advanced atherosclerosis, are characterized by an imbalance between pro-resolving and pro-inflammatory mediators, such as leukotrienes, leading to defective resolution of inflammation, tissue injury and damage-associated molecular pattern (DAMP)-mediated inflammation31–33.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [31]
Subendothelial retention of lipoproteins and immune cells in the vessel wall comprises the first stage of atherosclerosis.
“Subendothelial retention of lipoproteins and immune cells in the vessel wall comprises the first stage of atherosclerosis.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [23]
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- Authors
- Tabas, I.
- Affiliations
- Columbia University Irving Medical Center (US)
- Corresponding author
- Tabas, Ira
- ORCID
- Tabas, Ira
- Venue
- Nature Reviews Immunology
- Published
- 2009-12-04
- Volume
- 10
- Issue
- 1
- Pages
- 36-46
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- PMC
- PMC2854623
- OpenAlex
- W1964064254
- Cited by
- 1,120
- References
- 154
- Citations by year
- 2026: 37 · 2025: 38 · 2024: 50 · 2023: 47 · 2022: 59 · 2021: 70 · 2020: 71 · 2019: 84 · 2018: 68 · 2017: 79 · 2016: 78 · 2015: 83 · 2014: 85 · 2013: 80 · 2012: 88
- FWCI
- 4.97
- 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)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL-75662, P01HL054591, R01HL075662, HL 54591)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- atherosclerosis, inflammation resolution, macrophage cell death, efferocytosis, anti-inflammatory therapy, plaque progression
- MeSH terms
- Animals, Humans, Inflammation, Macrophage Activation, Macrophages, Phagocytosis, Apoptosis, Atherosclerosis
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