Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis (Review)
- Ben Ke
- Na Zhu
- Fuli Luo
- Yang Xu
- Xiangdong Fang
Affiliations: Department of Nephrology, The Third Hospital of Nanchang, Nanchang, Jiangxi 330009, P.R. China, Nanchang University School of Medicine, Nanchang, Jiangxi 330006, P.R. China, Department of Nephrology, Chinese Medicine Hospital in Jiangxi Province, Nanchang, Jiangxi 330006, P.R. China, Department of Nephrology, Jiangxi Provincial People's Hospital, Nanchang, Jiangxi 330006, P.R. China, Department of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China
- Published online on: June 13, 2017 https://doi.org/10.3892/mmr.2017.6762
Copyright: © Ke
et al. This is an open access article distributed under the
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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.