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Erschienen in: International Urology and Nephrology 7/2018

23.02.2018 | Nephrology - Original Paper

Renalase contributes to protection against renal fibrosis via inhibiting oxidative stress in rats

verfasst von: Yiru Wu, Liyan Wang, Xiaoqi Wang, Yahui Wang, Qidong Zhang, Wenhu Liu

Erschienen in: International Urology and Nephrology | Ausgabe 7/2018

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Abstract

Background

Renal interstitial fibrosis (RIF) is a common pathway for progression of chronic kidney disease (CKD) to end-stage renal disease. In our previous study, it has been provided that renalase can ameliorate renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats. The other mechanism of renalase to alleviate renal fibrosis should be explored.

Materials and methods

In this study, we evaluated the role of oxidative stress in UUO rats and epithelial–mesenchymal transition (EMT) in human proximal renal tubular epithelial (HK-2) cells and examined the association of renalase.

Results

Oxidative stress could induce EMT and fibrosis in HK-2 cells. In the UUO model, oxidative stress occurred and maintained at a high level leading to RIF. Administration of renalase by adenovirus significantly attenuated oxidative stress and further in vitro study showed that renalase can exert anti-fibrosis by inhibiting oxidative stress.

Conclusion

Our results prompt another mechanism of anti-fibrotic renal protection of renalase, which may be partly associated with inhibiting oxidative stress. These data provided another theoretical basis that supplementation with exogenous renalase may be a promising strategy for slowing or halting the progression of CKD.
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Metadaten
Titel
Renalase contributes to protection against renal fibrosis via inhibiting oxidative stress in rats
verfasst von
Yiru Wu
Liyan Wang
Xiaoqi Wang
Yahui Wang
Qidong Zhang
Wenhu Liu
Publikationsdatum
23.02.2018
Verlag
Springer Netherlands
Erschienen in
International Urology and Nephrology / Ausgabe 7/2018
Print ISSN: 0301-1623
Elektronische ISSN: 1573-2584
DOI
https://doi.org/10.1007/s11255-018-1820-2

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