Accumulation of advanced glycation end products promotes atrophic nonunion incidence in mice through a CtBP1/2-dependent mechanism.
Advanced glycation end products
Atrophic nonunion
C-terminal binding protein
Histone deacetylase 1
Runt-related transcription factor 2
Journal
Experimental cell research
ISSN: 1090-2422
Titre abrégé: Exp Cell Res
Pays: United States
ID NLM: 0373226
Informations de publication
Date de publication:
01 11 2023
01 11 2023
Historique:
received:
22
06
2023
revised:
13
08
2023
accepted:
01
09
2023
medline:
2
10
2023
pubmed:
12
9
2023
entrez:
11
9
2023
Statut:
ppublish
Résumé
Atrophic nonunion (AN) is a complex and poorly understood pathological condition resulting from impaired fracture healing. Advanced glycation end products (AGEs) have been implicated in the pathogenesis of several bone disorders, including osteoporosis and osteoarthritis. However, the role of AGEs in the development of AN remains unclear. This study found that mice fed a high-AGE diet had a higher incidence of atrophic nonunion (AN) compared to mice fed a normal diet following tibial fractures. AGEs induced two C-terminal binding proteins (CtBPs), CtBP1 and CtBP2, which were necessary for the development of AN in response to AGE accumulation. Feeding a high-AGE diet after fracture surgery in CtBP1/2
Identifiants
pubmed: 37696386
pii: S0014-4827(23)00313-0
doi: 10.1016/j.yexcr.2023.113765
pii:
doi:
Substances chimiques
Core Binding Factor Alpha 1 Subunit
0
Transcription Factors
0
Glycation End Products, Advanced
0
Receptor for Advanced Glycation End Products
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
113765Informations de copyright
Copyright © 2023 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no any financial or nonfinancial interests that might have influenced the performance or presentation of the work described in this manuscript.