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Journal of Diabetes Research
Volume 2017, Article ID 3560238, 6 pages
Review Article

Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy

1Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China
2Department of Medicine, Rhode Island Hospital and Alpert Medical School, Brown University, Providence, RI, USA

Correspondence should be addressed to Shougang Zhuang; gro.napsefil@gnauhzs

Received 30 November 2016; Accepted 20 February 2017; Published 23 April 2017

Academic Editor: Secundino Cigarran

Copyright © 2017 Na Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Diabetic nephropathy (DN), a leading cause of end-stage renal disease (ESRD), becomes a worldwide problem. Ultrastructural changes of the glomerular filtration barrier, especially the pathological changes of podocytes, lead to proteinuria in patients with diabetes. Podocytes are major components of glomerular filtration barrier, lining outside of the glomerular basement membrane (GBM) to maintain the permeability of the GBM. Autophagy is a high conserved cellular process in lysosomes including impaired protein, cell organelles, and other contents in the cytoplasm. Recent studies suggest that activation of autophagy in podocytes may be a potential therapy to prevent the progression of DN. Here, we review the mechanisms of autophagy in podocytes and discuss the current studies about alleviating proteinuria via activating podocyte autophagy.