The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Omega-3 Fatty Acids Prevent Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome Activation
Open accessAbstract
Omega-3 fatty acids (ω-3 FAs) have potential anti-inflammatory activity in a variety of inflammatory human diseases, but the mechanisms remain poorly understood. Here we show that stimulation of macrophages with ω-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1β secretion. In addition, G protein-coupled receptor 120 (GPR120) and GPR40 and their downstream scaffold protein β-arrestin-2 were shown to be involved in inflammasome inhibition induced by ω-3 FAs. Importantly, ω-3 FAs also prevented NLRP3 inflammasome-dependent inflammation and metabolic disorder in a high-fat-diet-induced type 2 diabetes model. Our results reveal a mechanism through which ω-3 FAs repress inflammation and prevent inflammation-driven diseases and suggest the potential clinical use of ω-3 FAs in gout, autoinflammatory syndromes, or other NLRP3 inflammasome-driven inflammatory diseases.
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“The anti-inflammatory effects of omega-3 fatty acids seems to be mediated by binding to the G-protein–coupled receptor 120 and inhibition of NLRP3 inflammasome activity (53,54).”
From Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms (2018) · cites this paper as [54]
Citations
Cites
A role for mitochondria in nlrp3 inflammasome activation
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Self-citationGout-associated uric acid crystals activate the NALP3 inflammasome
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Self-citationType 2 diabetes as an inflammatory disease
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Thioredoxin-interacting protein links oxidative stress to inflammasome activation
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Self-citationThe NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
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The Inflammasomes: Guardians of the Body
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Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling
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Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes
Esser, N., Legrand-Poels, S., Piette, J., Scheen, A. J., & Paquot, N. (2014) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2014.04.006 · Cited by 1,981
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Tilg, H., Zmora, N., Adolph, T. E., & Elinav, E. (2020) · Nature Reviews Immunology · doi:10.1038/s41577-019-0198-4 · Cited by 1,089
Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome
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Self-citationFranceschi, C., Garagnani, P., Vitale, G., Capri, M., & Salvioli, S. (2017) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2016.09.005 · Cited by 997
Metadata
- Authors
- Yan, Y., Jiang, W., Spinetti, T., Tardivel, A., Castillo, R., Bourquin, C., Guarda, G., Tian, Z., Tschopp, J., & Zhou, R.
- Affiliations
- University of Science and Technology of China (CN)
- University of Fribourg (CH)
- University of Lausanne (CH)
- Corresponding author
- Tian, Zhigang
- Zhou, Rongbin
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 38
- Issue
- 6
- Pages
- 1154-1163
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1998522372
- Cited by
- 784
- References
- 48
- Citations by year
- 2026: 53 · 2025: 65 · 2024: 55 · 2023: 68 · 2022: 51 · 2021: 77 · 2020: 51 · 2019: 63 · 2018: 70 · 2017: 63 · 2016: 57 · 2015: 57 · 2014: 36 · 2013: 17
- FWCI
- 24.95
- 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, 391 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
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Open Access CRIS of the University of Bern
- Funders
- National Natural Science Foundation of China (81222040, 31200659, 81273318, 91029303)
- Ministry of Education of the People's Republic of China (20123402110010, 20123402120001)
- University of Science and Technology of China
- Chinese Academy of Sciences
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Louis-Jeantet Foundation
- Fundamental Research Funds for the Central Universities
- Program for New Century Excellent Talents in University
- Seventh Framework Programme
- National Key Research and Development Program of China (2013CB944904)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- omega-3 fatty acids, NLRP3 inflammasome, caspase-1 activation, IL-1β secretion, macrophages, GPR120, GPR40, β-arrestin2, eicosapentaenoic acid, docosahexaenoic acid, type 2 diabetes, metabolic disorders, inflammation, gout, autoinflammatory disease, high-fat diet
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, beta-Arrestins, beta-Arrestin 2, Animals, Carrier Proteins, Cells, Cultured, Diabetes Mellitus, Type 2, Docosahexaenoic Acids, Enzyme Activation, Inflammation, Macrophages, Mice, Inbred C57BL, Eicosapentaenoic Acid, Fatty Acids, Omega-3, Mice, Knockout, Arrestins, Caspase 1, Receptors, G-Protein-Coupled, Mice, Interleukin-1beta, Inflammasomes, Diet, High-Fat
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