Myeloid AMPK signaling restricts fibrosis but is not required for metformin improvements during CDAHFD-induced NASH in mice.
Journal
Journal of lipid research
ISSN: 1539-7262
Titre abrégé: J Lipid Res
Pays: United States
ID NLM: 0376606
Informations de publication
Date de publication:
16 May 2024
16 May 2024
Historique:
received:
08
08
2023
revised:
07
05
2024
accepted:
11
05
2024
medline:
19
5
2024
pubmed:
19
5
2024
entrez:
18
5
2024
Statut:
aheadofprint
Résumé
Metabolic programming underpins inflammatory processes of immune cells. In the context of chronic liver disease, liver macrophage activation and response to hepatocellular damage is dependent on profound metabolic changes. Here, we sought to identify the role of an important metabolic regulator, AMP-activated protein kinase (AMPK), specifically within myeloid cells during the progression of non-alcoholic steatohepatitis (NASH) and whether treatment with metformin, a first line therapy for diabetes and activator of AMPK could stem disease progression. Male and female Prkaa1
Identifiants
pubmed: 38762124
pii: S0022-2275(24)00069-5
doi: 10.1016/j.jlr.2024.100564
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
100564Informations de copyright
Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.