Mast Cells Promote Nonalcoholic Fatty Liver Disease Phenotypes and Microvesicular Steatosis in Mice Fed a Western Diet.
Adolescent
Adult
Aged
Aged, 80 and over
Aldehyde Oxidoreductases
/ genetics
Animals
Biliary Tract
/ immunology
Diet, Western
/ adverse effects
Disease Models, Animal
Female
Gene Expression Regulation
/ immunology
Hepatocytes
/ pathology
Humans
Liver
/ immunology
Liver Cirrhosis
/ genetics
Male
Mast Cells
/ immunology
Mice
MicroRNAs
/ metabolism
Middle Aged
Non-alcoholic Fatty Liver Disease
/ genetics
Young Adult
Journal
Hepatology (Baltimore, Md.)
ISSN: 1527-3350
Titre abrégé: Hepatology
Pays: United States
ID NLM: 8302946
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
revised:
16
12
2020
received:
12
05
2020
accepted:
17
12
2020
pubmed:
13
1
2021
medline:
5
1
2022
entrez:
12
1
2021
Statut:
ppublish
Résumé
Nonalcoholic fatty liver disease (NAFLD) is simple steatosis but can develop into nonalcoholic steatohepatitis (NASH), characterized by liver inflammation, fibrosis, and microvesicular steatosis. Mast cells (MCs) infiltrate the liver during cholestasis and promote ductular reaction (DR), biliary senescence, and liver fibrosis. We aimed to determine the effects of MC depletion during NAFLD/NASH. Wild-type (WT) and Kit MCs promote WD-induced biliary and liver damage and may promote microvesicular steatosis development during NAFLD progression to NASH through miR-144-3p/ALDH1A3 signaling. Inhibition of MC activation may be a therapeutic option for NAFLD/NASH treatment.
Sections du résumé
BACKGROUND AND AIMS
Nonalcoholic fatty liver disease (NAFLD) is simple steatosis but can develop into nonalcoholic steatohepatitis (NASH), characterized by liver inflammation, fibrosis, and microvesicular steatosis. Mast cells (MCs) infiltrate the liver during cholestasis and promote ductular reaction (DR), biliary senescence, and liver fibrosis. We aimed to determine the effects of MC depletion during NAFLD/NASH.
APPROACH AND RESULTS
Wild-type (WT) and Kit
CONCLUSIONS
MCs promote WD-induced biliary and liver damage and may promote microvesicular steatosis development during NAFLD progression to NASH through miR-144-3p/ALDH1A3 signaling. Inhibition of MC activation may be a therapeutic option for NAFLD/NASH treatment.
Identifiants
pubmed: 33434322
doi: 10.1002/hep.31713
pmc: PMC9271361
mid: NIHMS1819811
doi:
Substances chimiques
MIRN144 microRNA, human
0
MIRN144 microRNA, mouse
0
MicroRNAs
0
Aldehyde Oxidoreductases
EC 1.2.-
aldehyde dehydrogenase (NAD(P)+)
EC 1.2.1.5
Types de publication
Journal Article
Observational Study
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
164-182Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK108959
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK054811
Pays : United States
Organisme : BLRD VA
ID : I01 BX000574
Pays : United States
Organisme : BLRD VA
ID : I01 BX001724
Pays : United States
Organisme : BLRD VA
ID : I01 BX003031
Pays : United States
Organisme : BLRD VA
ID : IK6 BX004601
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK119421
Pays : United States
Organisme : BLRD VA
ID : IK6 BX005226
Pays : United States
Informations de copyright
© 2021 by the American Association for the Study of Liver Diseases.
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