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ShareMar. 1, 2010 — A leading contributor to the development of both diseases that affect a structure in the kidney known as the glomerulus (glomerular diseases) and kidney failure is injury and loss of kidney cells known as podocytes.
New research, performed by Tobias Huber and colleagues, at University Hospital Freiburg, Germany, has now determined that podocyte integrity in mice is maintained by the cellular process autophagy.
In the study, mouse podocytes were found to naturally undergo high levels of autophagy. Furthermore, deletion of the gene autophagy-related 5 in podocytes led to podocyte loss and glomerular disease in aging mice and to increased susceptibility to models of glomerular disease in young mice.
The authors therefore suggest that autophagy helps protect against podocyte aging and glomerular injury and that it could be targeted to reduce human glomerular disease and aging-related loss of kidney function.
The research appears in the Journal of Clinical Investigation.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
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Journal Reference:
- björn Hartleben, Markus Gödel, Catherine Meyer-Schwesinger, Shuya Liu, Theresa Ulrich, Sven Köbler, Thorsten Wiech, Florian Grahammer, Sebastian J. Arnold, Maja T. Lindenmeyer, Clemens D. Cohen, Hermann Pavenstädt, Dontscho Kerjaschki, Noboru Mizushima, Andrey S. Shaw, Gerd Walz, and Tobias B. Huber. Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI39492
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