Journal
SEMINARS IN NEPHROLOGY
Volume 34, Issue 1, Pages 42-52Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2013.11.007
Keywords
Podocyte; kidney; autophagy; mTOR; ATG5; LC3; RAPTOR; FSGS; diabetic nephropathy; glomerulonephritis; lysosomal storage diseases
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Funding
- Deutsche Forschungsgemeinschaft
- Excellence Initiative of the German Federal and State Governments [EXC 294]
- GSC-4 Spemann Graduate School
- BMBF-Gerontosys II-NephAge
- Joint Transnational Grant
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Glomerular filtration coupled to tubular reabsorption was the prerequisite for one of the most important milestones in evolution, when animals made their way from water onto land. To fulfill the enormous filtration task the filter is composed of the most sophisticated postmitotic epithelial cells-the podocytes, which have only a very limited ability to regenerate. Podocyte injury and loss owing to genetic, toxic, immunologic, or metabolic insults underlie the most common glomerular diseases. Thus, the understanding of the factors and mechanisms that help to maintain podocytes are of major clinical importance. Recently, autophagy emerged as a key mechanism to eliminate unwanted cytoplasmic materials, thereby preventing cellular damage and stress to safeguard long-lived podocytes. Here, we highlight the accumulating evidence suggesting that autophagy plays a critical role in the homeostasis of podocytes during glomerular disease and aging. (C) 2014 Elsevier Inc. All rights reserved.
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