个人中心| | 帮助
高级检索
当前位置： 首页 > 详情页

Estrogen receptor β attenuates renal fibrosis by suppressing the transcriptional activity of Smad3

| 认领 | 导出 | |

文献详情

资源类型：
WOS体系：
Pubmed体系：

收录情况： ◇ SCIE

作者：
Cao Rong[1] * ; Su Wen[2] * ; Sheng Jingyi[3,11] ; Guo Yanlin[4] ; Su Jie[2] ; Zhang Cong[4] ; Wang Honglian[3] ; Tang Yizhe[5,13] ; Chen Lei[2] ; Qiao Rongfang[4] ; Chen Xiaocong[2] ; Huang Xiaoru[3,6] ; Zhou Yunfeng[7] ; Zhu Lizhen[2] ; Bai Zirui[2] ; Zhang Xiaoyan[8] ; Gustafsson Jan-Ake[9,10] ; Wan Qijun[1] ; Lan Hui-Yao[3] ; Guan Youfei[4] ;
机构： [1]Department of Nephrology, the First Affiliated Hospital of Shenzhen University, the Second People’s Hospital of Shenzhen, Shenzhen 518035, China [2]Shenzhen University Health Science Center, Department of Pathology, Shenzhen University, Shenzhen 518071, China [3]Department of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China [4]Advanced Institute for Medical Sciences, Dalian Medical University, Dalian 116044, Liaoning, China [5]The First Affiliated Hospital of Shenzhen University, Health Science Center, China [6]Guangdong-Hong Kong Joint Laboratory on Immunological and Genetic Kidney Diseases, Guangdong Academy of Medical Sciences, Guangdong Provincial People’s Hospital, Guangzhou 510080, China [7]Department of Physiology at the Basic Medical College, Shenzhen University Health Science Center, Shenzhen 518071, China [8]Health Science Center, East China Normal University, Shanghai 200241, China [9]Center for Innovative Medicine, Department of Biosciences and Nutrition, Karolinska Institute, Stockholm, Sweden [10]Center for Nuclear Receptors and Cell Signaling, University of Houston, Houston, USA [11]Jiangsu Key Laboratory for Biomaterials and Devices, School of Biological Sciences & Medical Engineering, Southeast University, Nanjing 210000, China [12]Research Center for Integrative Medicine, the Affiliated Traditional Medicine Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China [13]The Second People’s Hospital of Shenzhen, Institute of Translational Medicine, Medical Research Center, China
出处：
DOI： 10.1016/j.bbadis.2023.166755
ISSN：

关键词： CKD ERβ Tubular epithelial cells TGF-β Smad3

摘要：
Renal fibrosis (RF) is a common pathway leading to chronic kidney disease (CKD), which lacks effective treatment. While estrogen receptor beta (ERβ) is known to be present in the kidney, its role in RF remains unclear. The present study aimed to investigate the role and underlying mechanism of ERβ during RF progression in patients and animal models with CKD. We found that ERβ was highly expressed in the proximal tubular epithelial cells (PTECs) in healthy kidneys but its expression was largely lost in patients with immunoglobin A nephropathy (IgAN) and in mice with unilateral ureter obstruction (UUO) and subtotal nephrectomy (5/6Nx). ERβ deficiency markedly exacerbated, whereas ERβ activation by WAY200070 and DPN attenuated RF in both UUO and 5/6Nx mouse models, suggesting a protective role of ERβ in RF. In addition, ERβ activation inhibited TGF-β1/Smad3 signaling, while loss of renal ERβ was associated with overactivation of the TGF-β1/Smad3 pathway. Furthermore, deletion or pharmacological inhibition of Smad3 prevented the loss of ERβ and RF. Mechanistically, activation of ERβ competitively inhibited the association of Smad3 with the Smad-binding element, thereby downregulating the transcription of the fibrosis-related genes without altering Smad3 phosphorylation in vivo and in vitro. In conclusion, ERβ exerts a renoprotective role in CKD by blocking the Smad3 signaling pathway. Thus, ERβ may represent as a promising therapeutic agent for RF.Copyright © 2023. Published by Elsevier B.V.

基金：
This work was supported by Guangdong Basic and Applied Basic Research Foundation (2021A1515010991); The Shenzhen Science and Technology Project (JCYJ20210324103602006 & JCYJ202103240 94213037); The Shenzhen Second People’s Hospital Clinical Research Project (20223357004); The National Natural Science Foundation of China (No. 81600534, 81870405, 81970606, 81970595 & 82270703); The Shenzhen Key Medical Discipline Construction Fund (SZXK009); Research Grants Council of Hong Kong (14117418, 14104019, 14101121); The Guangdong-Hong Kong-Macao-Joint Labs Program from Guangdong Science and Technology Department (2019B121205005); The Lui Che Woo Institute of Innovative Medicine (CARE program); And the National Key Research and Development Program of China (2020YFC2005000).
语种：
外文
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2022]版：
大类 | 2 区 生物学
小类 | 1 区 生物物理 2 区 生化与分子生物学
最新[2025]版：
大类 | 2 区 生物学
小类 | 2 区 生物物理 3 区 生化与分子生物学
JCR分区：
出版当年[2021]版：
Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Q1 BIOPHYSICS
最新[2023]版：
Q1 BIOPHYSICS Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

第一作者：
第一作者机构： [1]Department of Nephrology, the First Affiliated Hospital of Shenzhen University, the Second People’s Hospital of Shenzhen, Shenzhen 518035, China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Cao Rong,Su Wen,Sheng Jingyi,et al.Estrogen receptor β attenuates renal fibrosis by suppressing the transcriptional activity of Smad3[J].BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE.2023,1869(6):doi:10.1016/j.bbadis.2023.166755.
APA：
Cao Rong,Su Wen,Sheng Jingyi,Guo Yanlin,Su Jie...&Guan Youfei.(2023).Estrogen receptor β attenuates renal fibrosis by suppressing the transcriptional activity of Smad3.BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE,1869,(6)
MLA：
Cao Rong,et al."Estrogen receptor β attenuates renal fibrosis by suppressing the transcriptional activity of Smad3".BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE 1869..6(2023)

相关文献

[1]Therapeutic Potential for Renal Fibrosis by targeting Smad3-dependent Non-coding RNAs [2]Petchiether A attenuates obstructive nephropathy by suppressing TGF-β/Smad3 and NF-κB signalling. [3]The effect of Smad2- and Smad3-targeting RNA interference on extracellular matrix synthesis in rat fibroblasts of peritoneal adhesion tissues. [4]Psoralen accelerates osteogenic differentiation of human bone marrow mesenchymal stem cells by activating the TGF-β/Smad3 pathway [5]Microarray Expression Profile of Exosomal circRNAs from High Glucose Stimulated Human Renal Tubular Epithelial Cells [6]MicroRNA profiling identifies miR-129-5p as a regulator of EMT in tubular epithelial cells. [7]Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production. [8]Deletion of Smad3 protects against C-reactive protein-induced renal fibrosis and inflammation in obstructive nephropathy. [9]Possible role of mitochondrial injury in Caulis Aristolochia manshuriensis-induced chronic aristolochic acid nephropathy. [10]Mitochondrial dysfunction is involved in aristolochic acid I-induced apoptosis in renal proximal tubular epithelial cells.

资源点击量：2018 今日访问量：0 总访问量：645 更新日期：2024-07-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 广东省中医院 技术支持：重庆聚合科技有限公司 地址：广州市越秀区大德路111号