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

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...

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Detalles Bibliográficos
Autores principales: Liu, Na, Xu, Liuqing, Shi, Yingfeng, Zhuang, Shougang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5420432/
https://www.ncbi.nlm.nih.gov/pubmed/28512641
http://dx.doi.org/10.1155/2017/3560238
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author Liu, Na
Xu, Liuqing
Shi, Yingfeng
Zhuang, Shougang
author_facet Liu, Na
Xu, Liuqing
Shi, Yingfeng
Zhuang, Shougang
author_sort Liu, Na
collection PubMed
description 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.
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spelling pubmed-54204322017-05-16 Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy Liu, Na Xu, Liuqing Shi, Yingfeng Zhuang, Shougang J Diabetes Res Review Article 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. Hindawi 2017 2017-04-23 /pmc/articles/PMC5420432/ /pubmed/28512641 http://dx.doi.org/10.1155/2017/3560238 Text en Copyright © 2017 Na Liu et al. http://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Review Article
Liu, Na
Xu, Liuqing
Shi, Yingfeng
Zhuang, Shougang
Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy
title Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy
title_full Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy
title_fullStr Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy
title_full_unstemmed Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy
title_short Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy
title_sort podocyte autophagy: a potential therapeutic target to prevent the progression of diabetic nephropathy
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5420432/
https://www.ncbi.nlm.nih.gov/pubmed/28512641
http://dx.doi.org/10.1155/2017/3560238
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