Dietary or pharmacological inhibition of insulin-like growth factor-1 protects from renal ischemia-reperfusion injury in mice.
Détails
Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_D61A8B942B5B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Dietary or pharmacological inhibition of insulin-like growth factor-1 protects from renal ischemia-reperfusion injury in mice.
Périodique
iScience
ISSN
2589-0042 (Electronic)
ISSN-L
2589-0042
Statut éditorial
Publié
Date de publication
20/12/2024
Peer-reviewed
Oui
Volume
27
Numéro
12
Pages
111256
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Publication Status: epublish
Résumé
One-week protein restriction (PR) limits ischemia-reperfusion (IR) damages and improves metabolic fitness. Similarly, longer-term calory restriction results in increased lifespan, partly via reduced insulin-like growth factor (IGF)-1. However, the influence of short-term PR on IGF-1 and its impact on IR are unknown. PR was achieved in mice via one-week carbohydrate loading and/or through a low-protein diet. PR decreased IGF-1 circulating levels as well as renal and hepatic expression. Upon renal IR, serum IGF-1 positively correlated with renal dysfunction and tissular damages, independently of sex and age. Exogenous IGF-1 administration abrogated PR benefits during IR, while IGF-1 receptor inhibition with linsitinib was protective. IGF-1 was associated with a reduction in forkhead box O (FoxO), and AMP-activated protein kinase (AMPK) signaling pathways previously demonstrated to improve IR resilience in various organs. These data support dietary or pharmacological reduction of IGF-1 signaling to mitigate IR injury prior to solid organ transplantation and beyond.
Mots-clé
Biochemistry, Biological sciences, Cellular physiology, Natural sciences, Pharmacology, Physiology
Pubmed
Web of science
Open Access
Oui
Financement(s)
Fonds national suisse
Fondation Leenaards
Création de la notice
19/12/2024 9:00
Dernière modification de la notice
25/01/2025 7:04