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Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis

Chronic kidney disease (CKD) has a very high mortality rate and remains a global health challenge. Inhibiting renal fibrosis is one of the most promising therapeutic strategies for CKD. Recent studies have indicated that endoplasmic reticulum stress (ERS) serves an active role in the development of...

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Detalles Bibliográficos
Autores principales: Ke, Ben, Zhu, Na, Luo, Fuli, Xu, Yang, Fang, Xiangdong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562070/
https://www.ncbi.nlm.nih.gov/pubmed/28627612
http://dx.doi.org/10.3892/mmr.2017.6762
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author Ke, Ben
Zhu, Na
Luo, Fuli
Xu, Yang
Fang, Xiangdong
author_facet Ke, Ben
Zhu, Na
Luo, Fuli
Xu, Yang
Fang, Xiangdong
author_sort Ke, Ben
collection PubMed
description Chronic kidney disease (CKD) has a very high mortality rate and remains a global health challenge. Inhibiting renal fibrosis is one of the most promising therapeutic strategies for CKD. Recent studies have indicated that endoplasmic reticulum stress (ERS) serves an active role in the development of acute and chronic kidney disease, especially with regards to renal fibrosis. In the current review, the authors summarize the latest understanding of the role of ERS during the onset of renal fibrosis. ERS promotes renal fibrosis through multiple signaling pathways, such as transforming growth factor-β, epithelial-mesenchymal transition and oxidative stress. In addition, ERS also causes podocyte damage, leading to increased proteinuria and the development of renal fibrosis in rat models. In conclusion, targeted inhibition of ERS may become a promising therapeutic strategy for renal fibrosis.
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spelling pubmed-55620702017-10-23 Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis Ke, Ben Zhu, Na Luo, Fuli Xu, Yang Fang, Xiangdong Mol Med Rep Review Chronic kidney disease (CKD) has a very high mortality rate and remains a global health challenge. Inhibiting renal fibrosis is one of the most promising therapeutic strategies for CKD. Recent studies have indicated that endoplasmic reticulum stress (ERS) serves an active role in the development of acute and chronic kidney disease, especially with regards to renal fibrosis. In the current review, the authors summarize the latest understanding of the role of ERS during the onset of renal fibrosis. ERS promotes renal fibrosis through multiple signaling pathways, such as transforming growth factor-β, epithelial-mesenchymal transition and oxidative stress. In addition, ERS also causes podocyte damage, leading to increased proteinuria and the development of renal fibrosis in rat models. In conclusion, targeted inhibition of ERS may become a promising therapeutic strategy for renal fibrosis. D.A. Spandidos 2017-08 2017-06-13 /pmc/articles/PMC5562070/ /pubmed/28627612 http://dx.doi.org/10.3892/mmr.2017.6762 Text en Copyright: © Ke et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Review
Ke, Ben
Zhu, Na
Luo, Fuli
Xu, Yang
Fang, Xiangdong
Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis
title Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis
title_full Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis
title_fullStr Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis
title_full_unstemmed Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis
title_short Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis
title_sort targeted inhibition of endoplasmic reticulum stress: new hope for renal fibrosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562070/
https://www.ncbi.nlm.nih.gov/pubmed/28627612
http://dx.doi.org/10.3892/mmr.2017.6762
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