Nrf2 signaling attenuates epithelial-to-mesenchymal transition and renal interstitial fibrosis via PI3K/Akt signaling pathways.


Journal

Experimental and molecular pathology
ISSN: 1096-0945
Titre abrégé: Exp Mol Pathol
Pays: Netherlands
ID NLM: 0370711

Informations de publication

Date de publication:
12 2019
Historique:
received: 15 02 2019
revised: 10 07 2019
accepted: 12 08 2019
pubmed: 27 8 2019
medline: 27 2 2020
entrez: 27 8 2019
Statut: ppublish

Résumé

Nrf2 constitutes a therapeutic reference point for renal fibrosis and chronic kidney diseases. Nrf2-related signaling pathways are recognized to temper endothelial-to-mesenchymal transition (EMT) in fibrotic tissue. Nevertheless, the mechanism by which Nrf2 mitigates renal interstitial fibrosis is imprecise. The relationship between Nrf2 and renal interstitial fibrosis was investigated using the unilateral ureteral obstruction (UUO) model of Nrf2 The Nrf2 The results we obtained demonstrate that Nrf2 signaling pathway may perhaps offset the development of EMT, prompted by TGF-β1 and renal interstitial fibrosis. Likewise, the anti-fibrotic effect of Nrf2 was imparted by the inactivation of PI3K/Akt signaling. From our discoveries, we deliver new insight related to the prevention and treatment of kidney fibrosis.

Sections du résumé

BACKGROUND
Nrf2 constitutes a therapeutic reference point for renal fibrosis and chronic kidney diseases. Nrf2-related signaling pathways are recognized to temper endothelial-to-mesenchymal transition (EMT) in fibrotic tissue. Nevertheless, the mechanism by which Nrf2 mitigates renal interstitial fibrosis is imprecise.
METHODS
The relationship between Nrf2 and renal interstitial fibrosis was investigated using the unilateral ureteral obstruction (UUO) model of Nrf2
RESULTS
The Nrf2
CONCLUSIONS
The results we obtained demonstrate that Nrf2 signaling pathway may perhaps offset the development of EMT, prompted by TGF-β1 and renal interstitial fibrosis. Likewise, the anti-fibrotic effect of Nrf2 was imparted by the inactivation of PI3K/Akt signaling. From our discoveries, we deliver new insight related to the prevention and treatment of kidney fibrosis.

Identifiants

pubmed: 31449784
pii: S0014-4800(19)30116-9
doi: 10.1016/j.yexmp.2019.104296
pii:
doi:

Substances chimiques

Cadherins 0
Fibronectins 0
NF-E2-Related Factor 2 0
Transforming Growth Factor beta1 0
Proto-Oncogene Proteins c-akt EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

104296

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Jun Wang (J)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Haobo Zhu (H)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Liqu Huang (L)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Xiaojiang Zhu (X)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Jintong Sha (J)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Guogen Li (G)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Geng Ma (G)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Wei Zhang (W)

Department of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.

Min Gu (M)

Department of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China. Electronic address: njmuwzj1990@hotmail.com.

Yunfei Guo (Y)

Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China. Electronic address: guozhaooso@163.com.cn.

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Classifications MeSH