Ke Ben, Zhu Na, Luo Fuli, Xu Yang, Fang Xiangdong
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.
Mol Med Rep. 2017 Aug;16(2):1014-1020. doi: 10.3892/mmr.2017.6762. Epub 2017 Jun 13.
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.
慢性肾脏病(CKD)死亡率极高,仍然是一项全球性的健康挑战。抑制肾纤维化是治疗CKD最具前景的策略之一。最近的研究表明,内质网应激(ERS)在急慢性肾脏病的发展中起积极作用,尤其是在肾纤维化方面。在本综述中,作者总结了对ERS在肾纤维化发病过程中作用的最新认识。ERS通过多种信号通路促进肾纤维化,如转化生长因子-β、上皮-间质转化和氧化应激。此外,ERS还会导致足细胞损伤,导致蛋白尿增加以及大鼠模型中肾纤维化的发展。总之,靶向抑制ERS可能成为治疗肾纤维化的一种有前景的策略。