The RAGE signaling in osteoporosis.


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
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

115044

Informations 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.

Auteurs

Jianguo Zhou (J)

Department of Joint Surgery, Ganzhou People's Hospital, Ganzhou 341000, China. Electronic address: zjg840818@163.com.

Shiwei Liu (S)

Department of Joint Surgery, Ganzhou People's Hospital, Ganzhou 341000, China.

Shengrong Bi (S)

Department of Joint Surgery, Ganzhou People's Hospital, Ganzhou 341000, China.

Weihao Kong (W)

Department of Joint Surgery, Ganzhou People's Hospital, Ganzhou 341000, China.

Rui Qian (R)

Department of Joint Surgery, Ganzhou People's Hospital, Ganzhou 341000, China.

Xunlu Xie (X)

Department of Pathology, Ganzhou People's Hospital, Ganzhou 341000, China.

Ming Zeng (M)

Department of Orthopedics, Ruijin Traditional Chinese Medicine Hospital, Ruijin 342500, China.

Xiaowei Jiang (X)

Department of Joint Surgery, Ningdu County People's Hospital, Ningdu 342800, China.

Zhibin Liao (Z)

Department of Joint Surgery, Ningdu County People's Hospital, Ningdu 342800, China.

Ming Shuai (M)

Department of Orthopedics, Chongyi County People's Hospital, Chongyi 341300, China.

Wei Liu (W)

Department of Orthopedics, Ningdu County Traditional Chinese Medicine Hospital, Ningdu 342800, China.

Long Cheng (L)

Department of Orthopedics, Ningdu County Traditional Chinese Medicine Hospital, Ningdu 342800, China.

Moujian Wu (M)

Department of Orthopedics, Xingguo County Traditional Chinese Medicine Hospital, Xingguo 342400, China.

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Classifications MeSH