Omega-3 pleiad: The multipoint anti-inflammatory strategy

Omega 3 (ω3) fatty acids have been described since the 1980s as promising anti-inflammatory substances. Prostaglandin and leukotriene modulation were exhaustively explored as the main reason for ω3 beneficial outcomes. However, during the early 2000s, after the human genome decoding advent, the nutr...

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Published in:Critical reviews in food science and nutrition 2024-05, Vol.64 (14), p.4817-4832
Main Authors: da Silva Batista, Ellencristina, Nakandakari, Susana Castelo Branco Ramos, Ramos da Silva, Adelino Sanchez, Pauli, José Rodrigo, Pereira de Moura, Leandro, Ropelle, Eduardo Rochete, Camargo, Enilton A., Cintra, Dennys Esper
Format: Article
Language:English
Subjects:
cellular signaling
chronic diseases
Crosstalk
Fatty acids
food science
G protein-coupled receptors
genome
Genomes
GPR120
humans
Immune system
Inflammasomes
Inflammation
Intracellular signalling
nutrigenomics
nutrition
Omega 3
prostaglandins
Sensitizing
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Summary:Omega 3 (ω3) fatty acids have been described since the 1980s as promising anti-inflammatory substances. Prostaglandin and leukotriene modulation were exhaustively explored as the main reason for ω3 beneficial outcomes. However, during the early 2000s, after the human genome decoding advent, the nutrigenomic approaches exhibited an impressive plethora of ω3 targets, now under the molecular point of view. Different G protein-coupled receptors (GPCRs) recognizing ω3 and its derivatives appear to be responsible for blocking inflammation and insulin-sensitizing effects. A new class of ω3-derived substances, such as maresins, resolvins, and protectins, increases ω3 actions. Inflammasome disruption, the presence of GPR120 on immune cell surfaces, and intracellular crosstalk signaling mediated by PPARγ compose the last discoveries regarding the multipoint anti-inflammatory targets for this nutrient. This review shows a detailed mechanistic proposal to understand ω3 fatty acid action over the inflammatory environment in the background of several chronic diseases.
ISSN:1040-8398
1549-7852
1549-7852
DOI:10.1080/10408398.2022.2146044