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Abstract
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.
Acknowledgments
We thank the Research Collaboratory for Structural Bioinformatics – Protein Data Bank (RCSB-PDB) and AlphaFold Protein Structure Database for the free use of tridimensional protein structures. We also thank all the members of the Nutritional Genomics Lab for their helpful discussions. EAC thanks to CNPq (Brazilian National Council for Scientific and Technological Development) for the scientific productivity fellowship (CNPq: 315369/2021-3). S.C.B.R.N and D.E.C thanks to “São Paulo Research Foundation – FAPESP,” by grants 2020/13443-1, 2019/13168-3 and 2019/13210-0, and CNPq: 312970/2022-6, which support all scientific investigations at the laboratory.
Disclosure statement
The authors are not aware of any affiliations, memberships, funding, or financial holdings that might be perceived as affecting the objectivity of this review.
Funding
The author(s) reported there is no funding associated with the work featured in this article.