Resolvin D1 Enhances Necroptotic Cell Clearance Through Promoting Macrophage Fatty Acid Oxidation and Oxidative Phosphorylation.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
/ pharmacology
AMP-Activated Protein Kinases
/ metabolism
Animals
Apoptosis
Docosahexaenoic Acids
/ metabolism
Fatty Acids
/ metabolism
Female
Macrophages
/ drug effects
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Necroptosis
/ physiology
Necrosis
Oxidative Phosphorylation
Phagocytosis
Plaque, Atherosclerotic
/ metabolism
Prostaglandins
/ metabolism
Protein Kinases
/ deficiency
atherosclerosis
macrophage
necroptosis
resolvin
thromboxane
Journal
Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803
Informations de publication
Date de publication:
03 2021
03 2021
Historique:
pubmed:
22
1
2021
medline:
16
3
2021
entrez:
21
1
2021
Statut:
ppublish
Résumé
Plaque necrosis is a key feature of defective resolution in atherosclerosis. Recent evidence suggests that necroptosis promotes plaque necrosis; therefore, we sought to determine how necroptotic cells (NCs) impact resolution programs in plaques. Approach and Results: To investigate the role(s) of necroptosis in advanced atherosclerosis, we used mice deficient of These results suggest that NCs derange resolution by limiting key SPMs and impairing the efferocytic repertoire of macrophages. Moreover, these findings provide a molecular mechanism for RvD1 in directing proresolving metabolic programs in macrophages and further suggests RvD1 as a potential therapeutic strategy to limit NCs in tissues. Graphic Abstract: A graphic abstract is available for this article.
Identifiants
pubmed: 33472399
doi: 10.1161/ATVBAHA.120.315758
pmc: PMC8174560
mid: NIHMS1662896
doi:
Substances chimiques
Fatty Acids
0
Prostaglandins
0
resolvin D1
0
Docosahexaenoic Acids
25167-62-8
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
76898-47-0
MLKL protein, mouse
EC 2.7.-
Protein Kinases
EC 2.7.-
AMP-Activated Protein Kinases
EC 2.7.11.31
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1062-1075Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL106173
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL141127
Pays : United States
Organisme : NIGMS NIH HHS
ID : P01 GM095467
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL153019
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007343
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM124133
Pays : United States
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