Autophagy in acute kidney injury and maladaptive kidney repair.
Acute kidney injury
Autophagy
Chronic kidney disease
Fibrosis
Maladaptive repair
Journal
Burns & trauma
ISSN: 2321-3868
Titre abrégé: Burns Trauma
Pays: England
ID NLM: 101651457
Informations de publication
Date de publication:
2023
2023
Historique:
received:
23
09
2022
revised:
30
11
2022
accepted:
20
12
2022
entrez:
25
1
2023
pubmed:
26
1
2023
medline:
26
1
2023
Statut:
epublish
Résumé
Acute kidney injury (AKI) is a major renal disease characterized by a sudden decrease in kidney function. After AKI, the kidney has the ability to repair, but if the initial injury is severe the repair may be incomplete or maladaptive and result in chronic kidney problems. Autophagy is a highly conserved pathway to deliver intracellular contents to lysosomes for degradation. Autophagy plays an important role in maintaining renal function and is involved in the pathogenesis of renal diseases. Autophagy is activated in various forms of AKI and acts as a defense mechanism against kidney cell injury and death. After AKI, autophagy is maintained at a relatively high level in kidney tubule cells during maladaptive kidney repair but the role of autophagy in maladaptive kidney repair has been controversial. Nonetheless, recent studies have demonstrated that autophagy may contribute to maladaptive kidney repair after AKI by inducing tubular degeneration and promoting a profibrotic phenotype in renal tubule cells. In this review, we analyze the role and regulation of autophagy in kidney injury and repair and discuss the therapeutic strategies by targeting autophagy.
Identifiants
pubmed: 36694860
doi: 10.1093/burnst/tkac059
pii: tkac059
pmc: PMC9867874
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
tkac059Informations de copyright
© The Author(s) 2023. Published by Oxford University Press.
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