Proresolving receptor tames inflammation in atherosclerosis.
Journal
The Journal of clinical investigation
ISSN: 1558-8238
Titre abrégé: J Clin Invest
Pays: United States
ID NLM: 7802877
Informations de publication
Date de publication:
15 12 2021
15 12 2021
Historique:
entrez:
15
12
2021
pubmed:
16
12
2021
medline:
24
12
2021
Statut:
ppublish
Résumé
Nonresolving inflammation contributes to the progression of atherosclerosis, a chronic disease characterized by the accumulation of lipid-rich arterial plaques infiltrated with immune cells. In this issue of the JCI, Arnardottir and Thul et al. report that GPR32, a receptor for proresolving lipid mediators including resolvin D1, was decreased in human atherosclerotic lesions and that overexpression of this human receptor in mice reduced lesion area and necrosis of atherosclerotic plaques. Mechanistically, GPR32 signaling blunted the production of proinflammatory cytokines, enhanced macrophage phagocytosis, and reduced leukocyte accumulation. These results suggest that therapeutic targeting of GPR32 could be an approach to resolving chronic inflammation in atherosclerosis.
Identifiants
pubmed: 34907914
pii: 155240
doi: 10.1172/JCI155240
pmc: PMC8670831
doi:
pii:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Comment
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIGMS NIH HHS
ID : P01 GM095467
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK122808
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL106173
Pays : United States
Commentaires et corrections
Type : CommentOn
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