Extracellular adenosine signaling in bone health and disease.
Journal
Current opinion in pharmacology
ISSN: 1471-4973
Titre abrégé: Curr Opin Pharmacol
Pays: England
ID NLM: 100966133
Informations de publication
Date de publication:
06 2023
06 2023
Historique:
received:
04
11
2022
revised:
29
01
2023
accepted:
13
03
2023
pmc-release:
01
06
2024
medline:
5
6
2023
pubmed:
13
4
2023
entrez:
12
4
2023
Statut:
ppublish
Résumé
Purinergic signaling is a key molecular pathway in the maintenance of bone health and regeneration. P1 receptor signaling, which is activated by extracellular adenosine, has emerged as a key metabolic pathway that regulates bone tissue formation, function, and homeostasis. Extracellular adenosine is mainly produced by ectonucleotidases, and alterations in the function of these enzymes or compromised adenosine generation can result in bone disorders, such as osteoporosis and impaired fracture healing. This mini review discusses the key role played by adenosine in bone health and how its alterations contribute to bone diseases, as well as potential therapeutic applications of exogenous adenosine to combat bone diseases like osteoporosis and injury.
Identifiants
pubmed: 37044008
pii: S1471-4892(23)00031-0
doi: 10.1016/j.coph.2023.102378
pmc: PMC10247430
mid: NIHMS1886032
pii:
doi:
Substances chimiques
Adenosine
K72T3FS567
Adenosine Triphosphate
8L70Q75FXE
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
102378Subventions
Organisme : NIA NIH HHS
ID : R01 AG074491
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR071552
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR079189
Pays : United States
Informations de copyright
Copyright © 2023 Elsevier Ltd. 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.
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