Targeting hepatic oxidative stress rescues bone loss in liver fibrosis.
Chronic liver diseases
Hepatic osteodystrophy
Interleukin 17
Neutrophils
Reactive oxidative species
Stanniocalcin 1
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
12 2022
12 2022
Historique:
received:
09
03
2022
revised:
01
09
2022
accepted:
09
09
2022
pubmed:
17
9
2022
medline:
21
12
2022
entrez:
16
9
2022
Statut:
ppublish
Résumé
Chronic liver diseases often involve metabolic damage to the skeletal system. The underlying mechanism of bone loss in chronic liver diseases remains unclear, and appropriate therapeutic options, except for orthotopic liver transplantation, have proved insufficient for these patients. This study aimed to investigate the efficacy and mechanism of transplantation of immature hepatocyte-like cells converted from stem cells from human exfoliated deciduous teeth (SHED-Heps) in bone loss of chronic liver fibrosis. Mice that were chronically treated with CCl SHED-Hep transplantation (SHED-HepTx) improved trabecular bone loss and liver fibrosis in chronic CCl These findings suggest that targeting hepatic ROS provides a novel approach to treat bone loss resulting from chronic liver diseases.
Identifiants
pubmed: 36113772
pii: S2212-8778(22)00168-5
doi: 10.1016/j.molmet.2022.101599
pmc: PMC9515604
pii:
doi:
Substances chimiques
Interleukin-17
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101599Informations de copyright
Copyright © 2022 The Author(s). Published by Elsevier GmbH.. All rights reserved.