Pin1 Plays Essential Roles in NASH Development by Modulating Multiple Target Proteins.
Adipose Tissue
/ metabolism
Animals
Biomarkers
Disease Susceptibility
Genetic Predisposition to Disease
Humans
Isoenzymes
Lipid Metabolism
Liver Cirrhosis
/ etiology
NADPH Oxidases
/ metabolism
NIMA-Interacting Peptidylprolyl Isomerase
/ genetics
Non-alcoholic Fatty Liver Disease
/ etiology
Obesity
/ etiology
Reactive Oxygen Species
/ metabolism
NAFLD
NASH
Pin1
fibrosis
inflammation
lipid
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
29 11 2019
29 11 2019
Historique:
received:
15
10
2019
revised:
21
11
2019
accepted:
26
11
2019
entrez:
5
12
2019
pubmed:
5
12
2019
medline:
1
8
2020
Statut:
epublish
Résumé
Pin1 is one of the three known prolyl-isomerase types and its hepatic expression level is markedly enhanced in the obese state. Pin1 plays critical roles in favoring the exacerbation of both lipid accumulation and fibrotic change accompanying inflammation. Indeed, Pin1-deficient mice are highly resistant to non-alcoholic steatohepatitis (NASH) development by either a high-fat diet or methionine-choline-deficient diet feeding. The processes of NASH development can basically be separated into lipid accumulation and subsequent fibrotic change with inflammation. In this review, we outline the molecular mechanisms by which increased Pin1 promotes both of these phases of NASH. The target proteins of Pin1 involved in lipid accumulation include insulin receptor substrate 1 (IRS-1), AMP-activated protein kinase (AMPK) and acetyl CoA carboxylase 1 (ACC1), while the p60 of the NF-kB complex and transforming growth factor β (TGF-β) pathway appear to be involved in the fibrotic process accelerated by Pin1. Interestingly, Pin1 deficiency does not cause abnormalities in liver size, appearance or function. Therefore, we consider the inhibition of increased Pin1 to be a promising approach to treating NASH and preventing hepatic fibrosis.
Identifiants
pubmed: 31795496
pii: cells8121545
doi: 10.3390/cells8121545
pmc: PMC6952946
pii:
doi:
Substances chimiques
Biomarkers
0
Isoenzymes
0
NIMA-Interacting Peptidylprolyl Isomerase
0
Reactive Oxygen Species
0
NADPH Oxidases
EC 1.6.3.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The author declares no conflict of interest.
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