RIP Kinases in Liver Cell Death, Inflammation and Cancer.
apoptosis
hepatocellular carcinoma
liver disease
necroptosis
receptor-interacting protein kinase
Journal
Trends in molecular medicine
ISSN: 1471-499X
Titre abrégé: Trends Mol Med
Pays: England
ID NLM: 100966035
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
31
08
2018
revised:
16
10
2018
accepted:
17
10
2018
pubmed:
21
11
2018
medline:
18
6
2019
entrez:
21
11
2018
Statut:
ppublish
Résumé
Cell death is intrinsically linked to inflammatory liver disease and cancer development. Recent genetic studies have suggested that receptor-interacting protein kinase (RIPK)1 is implicated in liver disease pathogenesis by regulating caspase-dependent hepatocyte apoptosis induced by tumor necrosis factor (TNF) or other stimuli. In contrast, the contribution of caspase-independent RIPK3/mixed lineage kinase like (MLKL)-mediated hepatocyte necroptosis remains debatable. Hepatocyte apoptosis depends on the balance between RIPK1 prosurvival scaffolding functions and its kinase-activity-mediated proapoptotic function. Several regulatory steps promote the prosurvival role of RIPK1, including phosphorylation and ubiquitination of RIPK1 itself and other molecules involved in RIPK1 signaling. Pharmacological inhibition of liver damage by targeting RIPK1 signaling emerges as a potential therapeutic strategy to prevent chronic liver inflammation and hepatocarcinogenesis.
Identifiants
pubmed: 30455045
pii: S1471-4914(18)30203-X
doi: 10.1016/j.molmed.2018.10.007
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
47-63Informations de copyright
Copyright © 2018 Elsevier Ltd. All rights reserved.