OTUD6A in tubular epithelial cells mediates angiotensin II-induced kidney injury by targeting STAT3-Reference-Cited by-同舟云学术

OTUD6A in tubular epithelial cells mediates angiotensin II-induced kidney injury by targeting STAT3

Published:2024-02-01 Issue:2 Volume:326 Page:C400-C413
ISSN:0363-6143
Container-title:American Journal of Physiology-Cell Physiology
language:en
Short-container-title:American Journal of Physiology-Cell Physiology

Author:

Sun Xiaoyu¹²³,Chen Shuhong²,Zhao Ying⁴,Wu Tong²,Zhao Zheyu²,Luo Wu⁴,Han Jibo⁴,Fang Zimin⁴,Ye Bozhi⁴,Cao Gang⁵,Huang Shengbin²³^ORCID,Liang Guang¹⁴^ORCID

Affiliation:

1. Affiliated Yongkang First People’s Hospital and School of Pharmacy, Hangzhou Medical College, Hangzhou, People’s Republic of China

2. Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, People’s Republic of China

3. Department of Periodontics and Prosthodontics, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, People’s Republic of China

4. Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, People’s Republic of China

5. School of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China

Abstract

Ovarian tumor domain-containing protein 6 A (OTUD6A) knockout mice are protected against angiotensin II-induced kidney dysfunction and fibrosis. OTUD6A promotes pathological kidney remodeling and dysfunction by deubiquitinating signal transducer and activator of transcription 3 (STAT3). OTUD6A binds to and removes K63-linked-ubiquitin chains of STAT3 to promote its phosphorylation and activation, and subsequently enhances kidney fibrosis.

Funder

MOST | NSFC | NSFC-Zhejiang Joint Fund | 浙江省科学技术厅 | Basic Public Welfare Research Program of Zhejiang Province

MOST | National Natural Science Foundation of China

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpcell.00394.2023

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