Human proximal tubular epithelial cell-derived small extracellular vesicles mediate synchronized tubular ferroptosis in hypoxic kidney injury.
AKI-to-CKD transition
Ferroptosis
Hypoxia
Lipid peroxidation
Proximal tubular epithelial cells
Small extracellular vesicles
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
14 Jan 2024
14 Jan 2024
Historique:
received:
15
11
2023
accepted:
12
01
2024
medline:
21
1
2024
pubmed:
21
1
2024
entrez:
20
1
2024
Statut:
aheadofprint
Résumé
Hypoxia is the key pathobiological trigger of tubular oxidative stress and cell death that drives the transition of acute kidney injury (AKI) to chronic kidney disease (CKD). The mitochondrial-rich proximal tubular epithelial cells (PTEC) are uniquely sensitive to hypoxia and thus, are pivotal in propagating the sustained tubular loss of AKI-to-CKD transition. Here, we examined the role of PTEC-derived small extracellular vesicles (sEV) in propagating the 'wave of tubular death'. Ex vivo patient-derived PTEC were cultured under normoxia (21 % O
Identifiants
pubmed: 38244399
pii: S2213-2317(24)00018-1
doi: 10.1016/j.redox.2024.103042
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
103042Informations de copyright
Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors report no conflicts of interest.