Journal
AUTOPHAGY
Volume 8, Issue 5, Pages 826-837Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.19419
Keywords
autophagy; kidney tubule system; acute kidney injury; Atg5; p62
Categories
Funding
- DFG (Deutsche Forschungsgemeinschaft) [KFO 201]
- Excellence Initiative of German Federal Government [EXC 294]
- Excellence Initiative of German State Government [EXC 294]
- Spemann Graduate School [GSC-4]
- BMBF GerontosysII-NephAge [031589GA]
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Autophagy is responsible for the degradation of protein aggregates and damaged organelles. Several studies have reported increased autophagic activity in tubular cells after kidney injury. Here, we examine the role of tubular cell autophagy in vivo under both physiological conditions and stress using two different tubular-specific Atg5-knockout mouse models. While Atg5 deletion in distal tubule cells does not cause a significant alteration in kidney function, deleting Atg5 in both distal and proximal tubule cells results in impaired kidney function. Already under physiological conditions, Atg5-null tubule cells display a significant accumulation of p62 and oxidative stress markers. Strikingly, tubular cell Atg5-deficiency dramatically sensitizes the kidneys to ischemic injury, resulting in impaired kidney function, accumulation of damaged mitochondria as well as increased tubular cell apoptosis and proliferation, highlighting the critical role that autophagy plays in maintaining tubular cell integrity during stress conditions.
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