Smad3-Targeted Therapy Protects against Cisplatin-Induced AKI by Attenuating Programmed Cell Death and Inflammation via a NOX4-Dependent Mechanism

Smad3-Targeted Therapy Protects against Cisplatin-Induced AKI by Attenuating Programmed Cell Death and Inflammation via a NOX4-Dependent Mechanism

Background: Transforming growth factor-β (TGF-β)/Smad signaling is the central mediator in renal fibrosis, yet its functional role in acute kidney injury (AKI) is not fully understood. Recent evidence showed that TGF-β/Smad3 may be involved in the pathogenesis of AKI, but its functional role and mec...

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Bibliographic Details
Main Authors: Qin Yang, Li Gao, Xiao-wei Hu, Jia-nan Wang, Yao Zhang, Yu-hang Dong, Hui Yao Lan, Xiao-ming Meng
Format: Article
Language:English
Published: Karger Publishers 2021-02-01
Series:Kidney Diseases
Subjects:
acute kidney injury
cisplatin
smad3
nox4
programmed cell death
inflammation
Online Access:https://www.karger.com/Article/FullText/512986

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