The RAGE signaling in osteoporosis.
AGEs
Aβ
HMGB1
Osteoblasts
Osteoclastogenesis
Osteoporosis
RAGE
S100
Journal
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
ISSN: 1950-6007
Titre abrégé: Biomed Pharmacother
Pays: France
ID NLM: 8213295
Informations de publication
Date de publication:
Sep 2023
Sep 2023
Historique:
received:
14
05
2023
revised:
16
06
2023
accepted:
20
06
2023
medline:
17
8
2023
pubmed:
25
6
2023
entrez:
24
6
2023
Statut:
ppublish
Résumé
Osteoporosis (OP), characterized by an imbalance of bone remodeling between formation and resorption, has become a health issue worldwide. The receptor for advanced glycation end product (RAGE), a transmembrane protein in the immunoglobin family, has multiple ligands and has been involved in many chronic diseases, such as diabetes and OP. Increasing evidence shows that activation of the RAGE signaling negatively affects bone remodeling. Ligands, such as advanced glycation end products (AGEs), S100, β-amyloid (Aβ), and high mobility group box 1 (HMGB1), have been well documented that they may negatively regulate the proliferation and differentiation of osteoblasts and positively stimulate osteoclastogenesis by activating the expression of RAGE. In this review, we comprehensively discuss the structure of RAGE and its biological functions in the pathogenesis of OP. The research findings suggest that RAGE signaling has become a potential target for the therapeutic management of OP.
Identifiants
pubmed: 37354815
pii: S0753-3322(23)00834-X
doi: 10.1016/j.biopha.2023.115044
pii:
doi:
Substances chimiques
Receptor for Advanced Glycation End Products
0
Ligands
0
Glycation End Products, Advanced
0
HMGB1 Protein
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
115044Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.