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Atherosclerosis: evidence for impairment of resolution of vascular inflammation governed by specific lipid mediators
Open accessAbstract
Atherosclerosis is now recognized as an inflammatory disease involving the vascular wall. Recent results indicate that acute inflammation does not simply passively resolve as previously assumed but is actively terminated by a homeostatic process that is governed by specific lipid‐derived mediators initiated by lipoxygenases. Experiments with animals and humans support a proinflammatory role for the 5‐lipoxygenase system. In contrast, results from animal experiments showa range of responses with the 12/15‐lipoxygenase pathways in atherosclerosis. To date, the only two clinical epidemiology human studies both support an antiatherogenic role for 12/15‐lipoxygenase downstream actions. We tested the hypothesis that atherosclerosis results from a failure in the resolution of local inflammation by analyzing apolipoprotein E‐deficient mice with 1 ) global leukocyte 12/15‐lipoxygenase deficiency, 2 ) normal enzyme expression, or 3 ) macrophage‐specific 12/15‐lipoxygenase overexpression. Results from these indicate that 12/15‐lipoxy‐genase expression protects mice against atherosclerosis via its role in the local biosynthesis of lipid mediators, including lipoxin A 4 , resolvin D1, and protectin D1. These mediators exert potent agonist actions on macrophages and vascular endothelial cells that can control the magnitude of the local inflammatory response. Taken together, these findings suggest that a failure of local endogenous resolution mechanisms may underlie the unremitting inflammation that fuels atherosclerosis.—Merched, A. J., Ko, K., Gotlinger, K. H., Serhan, C. N. Chan, L. Atherosclerosis: evidence for impairment of resolution of vascular inflammation governed by specific lipid mediators. FASEB J. 22, 3595–3606 (2008)
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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 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 [32]
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Metadata
- Authors
- Merched, A. J., Ko, K., Gotlinger, K. H., Serhan, C. N., & Chan, L.
- Affiliations
- Baylor St. Luke's Medical Center (US)
- Brigham and Women's Hospital (US)
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2008-06-17
- Volume
- 22
- Issue
- 10
- Pages
- 3595-3606
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC2537438
- OpenAlex
- W2074102438
- Cited by
- 414
- References
- 55
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 9 · 2023: 20 · 2022: 14 · 2021: 23 · 2020: 22 · 2019: 17 · 2018: 36 · 2017: 27 · 2016: 32 · 2015: 31 · 2014: 30 · 2013: 28 · 2012: 22
- FWCI
- 27.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association (0465093Y, 0730172N)
- National Institutes of Health (P50 DE016191, HL‐51586)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- atherosclerosis, inflammation resolution, lipid mediators, 12/15-lipoxygenase, 5-lipoxygenase, lipoxin A4, resolvin D1, protectin D1, macrophages, vascular inflammation, ApoE-deficient mice
- MeSH terms
- Animals, Apolipoproteins E, Arachidonate 12-Lipoxygenase, Arachidonate 15-Lipoxygenase, Docosahexaenoic Acids, Endothelium, Vascular, Humans, Interleukins, Macrophages, Vasculitis, Mice, Knockout, Lipoxins, Atherosclerosis, Mice
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