Document Detail


Autophagy plays a critical role in kidney tubule maintenance, aging and ischemia-reperfusion injury.
MedLine Citation:
PMID:  22617445     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
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.
Authors:
Shuya Liu; Björn Hartleben; Oliver Kretz; Thorsten Wiech; Peter Igarashi; Noboru Mizushima; Gerd Walz; Tobias B Huber
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-5-01
Journal Detail:
Title:  Autophagy     Volume:  8     ISSN:  1554-8635     ISO Abbreviation:  -     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-5-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Renal Division; University Hospital Freiburg; Freiburg, Germany; Spemann Graduate School of Biology and Medicine (SGBM); Albert-Ludwigs-University; Freiburg, Germany; Faculty of Biology; Albert-Ludwigs-University; Freiburg, Germany.
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