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Semin Nephrol. 2014 Jan;34(1):42-52. doi: 10.1016/j.semnephrol.2013.11.007. Epub 2013 Nov 22.

Autophagy in glomerular health and disease.

Author information

1
Renal Division, University Hospital Freiburg, Freiburg, Germany; Institute of Pathology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
2
Renal Division, University Hospital Freiburg, Freiburg, Germany; Spemann Graduate School of Biology and Medicine, Albert Ludwigs University, Freiburg, Germany; Faculty of Biology, Albert Ludwigs University, Freiburg, Germany.
3
Renal Division, University Hospital Freiburg, Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, Albert Ludwigs University, Freiburg, Germany. Electronic address: tobias.huber@uniklinik-freiburg.de.

Abstract

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.

KEYWORDS:

ATG5; FSGS; LC3; Podocyte; RAPTOR; autophagy; diabetic nephropathy; glomerulonephritis; kidney; lysosomal storage diseases; mTOR

[Indexed for MEDLINE]

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