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10.4161/auto.19419

http://scihub22266oqcxt.onion/10.4161/auto.19419
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22617445!ä!22617445

suck abstract from ncbi


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pmid22617445      Autophagy 2012 ; 8 (5): 826-37
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  • Autophagy plays a critical role in kidney tubule maintenance, aging and ischemia-reperfusion injury #MMPMID22617445
  • Liu S; Hartleben B; Kretz O; Wiech T; Igarashi P; Mizushima N; Walz G; Huber TB
  • Autophagy 2012[May]; 8 (5): 826-37 PMID22617445show ga
  • 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.
  • |*Autophagy[MESH]
  • |Adaptor Proteins, Signal Transducing/metabolism[MESH]
  • |Aging/*pathology[MESH]
  • |Animals[MESH]
  • |Autophagy-Related Protein 5[MESH]
  • |Biomarkers/metabolism[MESH]
  • |Creatinine/blood[MESH]
  • |Embryo, Mammalian/abnormalities/pathology[MESH]
  • |Gene Deletion[MESH]
  • |Gene Knockout Techniques[MESH]
  • |Heat-Shock Proteins/metabolism[MESH]
  • |Kidney Tubules/abnormalities/metabolism/*pathology/ultrastructure[MESH]
  • |Mice[MESH]
  • |Microtubule-Associated Proteins/deficiency/metabolism[MESH]
  • |Organ Specificity[MESH]
  • |Oxidative Stress[MESH]
  • |Reperfusion Injury/blood/*pathology[MESH]
  • |Sequestosome-1 Protein[MESH]


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