Hepatic growth hormone - JAK2 - STAT5 signalling: Metabolic function, non-alcoholic fatty liver disease and hepatocellular carcinoma progression.
Animals
Carcinoma, Hepatocellular
/ genetics
Disease Models, Animal
Disease Progression
Growth Hormone
/ metabolism
Humans
Janus Kinase 2
/ genetics
Lipid Metabolism
Liver Neoplasms
/ genetics
Mice
Non-alcoholic Fatty Liver Disease
/ genetics
Receptors, Glucocorticoid
/ metabolism
STAT5 Transcription Factor
/ genetics
Signal Transduction
/ genetics
Hepatic lipid metabolism
Liver
Liver cancer
NAFLD
Journal
Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
31
08
2018
revised:
05
10
2018
accepted:
11
10
2018
pubmed:
6
11
2018
medline:
28
8
2020
entrez:
4
11
2018
Statut:
ppublish
Résumé
The rising prevalence of obesity came along with an increase in associated metabolic disorders in Western countries. Non-alcoholic fatty liver disease (NAFLD) represents the hepatic manifestation of the metabolic syndrome and is linked to primary stages of liver cancer development. Growth hormone (GH) regulates various vital processes such as energy supply and cellular regeneration. In addition, GH regulates various aspects of liver physiology through activating the Janus kinase (JAK) 2- signal transducer and activator of transcription (STAT) 5 pathway. Consequently, disrupted GH - JAK2 - STAT5 signaling in the liver alters hepatic lipid metabolism and is associated with NAFLD development in humans and mouse models. Interestingly, while STAT5 as well as JAK2 deficiency correlates with hepatic lipid accumulation, recent studies suggest that these proteins have unique ambivalent functions in chronic liver disease progression and tumorigenesis. In this review, we focus on the consequences of altered GH - JAK2 - STAT5 signaling for hepatic lipid metabolism and liver cancer development with an emphasis on lessons learned from genetic knockout models.
Identifiants
pubmed: 30389231
pii: S1043-4666(18)30398-3
doi: 10.1016/j.cyto.2018.10.010
pii:
doi:
Substances chimiques
Receptors, Glucocorticoid
0
STAT5 Transcription Factor
0
Growth Hormone
9002-72-6
Janus Kinase 2
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
154569Subventions
Organisme : NIAID NIH HHS
ID : R21 AI103388
Pays : United States
Informations de copyright
Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.