Lipoxin and resolvin receptors transducing the resolution of inflammation in cardiovascular disease.
- 1Karolinska Institutet (KI), Sweden
- 2INSERM U1116 Défaillance cardiovasculaire aiguë et chronique, France
A non-resolving inflammation results in a chronic inflammatory response, characteristic of atherosclerosis, abdominal aortic aneurysms and several other cardiovascular diseases. Restoring the levels specialized proresolving mediators to drive the chronic cardiovascular inflammation towards resolution is emerging as a novel therapeutic principle. The lipid mediators lipoxins and resolvins exert their proresolving actions through specific G-protein coupled receptors (GPCR). So far, four GPCR have been identified as the receptors for lipoxin A4 and the D- and E-series of resolvins, namely ALX/FPR2, DRV1/ GPR32, DRV2/GPR18, and ERV1/ChemR23. At the same time other pro-inflammatory ligands also activate some of these receptors. Recent studies of genetic targeting of these receptors in atherosclerotic mouse strains have revealed a major role for prereolving receptors in atherosclerosis. The present review addresses the complex pharmacology of these four proresolving GPCRs with focus on their therapeutic implications and opportunities for inducing the resolution of inflammation in cardiovascular disease.
Keywords: Artherosclerosis, ChemR23 receptor, FPR2/ALX receptor, Inflammation, Lipoxygenase
Received: 27 Jul 2018;
Accepted: 18 Oct 2018.
Edited by:Trinidad Montero-Melendez, Queen Mary University of London, United Kingdom
Reviewed by:Vincenzo BRANCALEONE, University of Basilicata, Italy
Jianmin Chen, Queen Mary University of London, United Kingdom
Copyright: © 2018 Bäck and Pirault. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Prof. Magnus Bäck, Karolinska Institutet (KI), Solna, Sweden, Magnus.Back@ki.se