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Implications of autophagy for glomerular aging and disease

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Abstract

Glomerular diseases lead to a progressive decline in renal function and account for the vast majority of end-stage kidney diseases. Injury and loss of glomerular podocytes are common determining factors of glomerular disease progression and renal failure. Podocytes are a primary glomerular target of toxic, immune, metabolic, and oxidant stress, but little is known of the factors that counteract cellular stress signaling pathways. This review focuses on recent findings that identify autophagy as a critical homeostatic and quality control mechanism maintaining glomerular homeostasis.

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Acknowledgements

We apologize to those colleagues whose work has not been cited because of imposed restrictions on article length. We thank Beate Vollenbröker, Wibke Bechtel, and Björn Hartleben for critically reading the manuscript and all members of our laboratories for their support and helpful discussions.

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Correspondence to Thomas Weide or Tobias B. Huber.

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This work is supported by a DFG grant to T.W. (PA 483/16-1), by DFG grants to T.B.H. (HU 1016/2-1, P7-KFO 201), and by the Excellence Initiative of the German Federal and State Governments (EXC 294).

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Weide, T., Huber, T.B. Implications of autophagy for glomerular aging and disease. Cell Tissue Res 343, 467–473 (2011). https://doi.org/10.1007/s00441-010-1115-0

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