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ABSTRACT: Background
The role of proximal tubular autophagy in repairing kidney injury following ischemia remains unclear.Methods
In this study, we utilized mice with conditional deletion of the Atg5 gene in proximal tubules and monitored the long-term dynamic regulation of autophagy following ischemic acute kidney injury (AKI).Results
The results showed that Atg5-deficient proximal tubule epithelial cells exhibited damaged mitochondria, concentric membranes, and lysosomal accumulation 24 h after ischemia/reperfusion. However, 28 days after ischemia/reperfusion, concentric membrane bodies remained, but lysosomal accumulation was no longer observed. Notably, the absence of Atg5 in renal tubular epithelial cells impaired renal function and led to increased tubular cell prolifer
SUBMITTER: Gong Y
PROVIDER: S-EPMC11619129 | biostudies-literature | 2024 Dec
REPOSITORIES: biostudies-literature