Dietary or pharmacological inhibition of insulin-like growth factor-1 protects from renal ischemia-reperfusion injury in mice.

Détails

Ressource 1Télécharger: 111256.pdf (4593.80 [Ko])
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
Auteur⸱e⸱s
Lyon A., Agius T., Macarthur M.R., Kiesworo K., Stavart L., Allagnat F., Mitchell S.J., Riella L.V., Uygun K., Yeh H., Déglise S., Golshayan D., Longchamp A.
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
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
Données d'usage