个人中心| | 帮助
高级检索
当前位置： 首页 > 详情页

Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production.

| 认领 | 导出 | |

文献详情

资源类型：
Pubmed体系：
作者：
Wang Jia-Nan[1] * ; Yang Qin[1] * ; Yang Chen[2] * ; Cai Yu-Ting[1,3] * ; Xing Tian[4] ; Gao Li[1] ; Wang Fang[1] ; Chen Xin[1] ; Liu Xue-Qi[1,3] ; He Xiao-Yan[1] ; Wei Biao[1] ; Jiang Ling[1,3] ; Li Chao[1] ; Jin Juan[5] ; Wen Jia-Gen[1] ; Ma Tao-Tao[1] ; Chen Hai-Yong[6] ; Li Jun[1] ; Meng Xiao-Ming[1,*1] ;
机构： [1]The Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, The Key Laboratory of Antiinflammatory and Immune Medicines, Ministry of Education, Hefei, 230032, China [2]Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, 524001, China [3]Department of Nephrology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230032, China [4]College & Hospital of Stomatology, Anhui Medical University, Key Lab. of Oral Diseases Research of Anhui Province, Hefei, 230032, China [5]Department of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China [6]School of Chinese Medicine, The University of Hong Kong, Hong Kong, China
出处：
DOI： 10.1016/j.redox.2020.101479

关键词： Smad TGF-β Diabetic nephropathy AKI Inflammation Oxidative stress

摘要：
The incidence and severity of acute kidney injury (AKI) is increased yearly in diabetic patients. Although the mechanisms for this remain unclear, the prevention of AKI in diabetic nephropathy is feasible and of value. As we detected highly activation of TGF-β/Smad3 signaling in both human biopsy and mouse model of diabetic nephropathy, we hypothesized that Smad3 activation in diabetic kidneys may increase AKI sensitivity. We tested our hypothesis in vitro using TGF-β type II receptor (TGF-βRII) disrupted tubular epithelial cells (TECs) and in vivo in mice with streptozotocin (STZ)-induced diabetic nephropathy before the induction of ischemia/reperfusion (I/R) injury. We found that high glucose (HG)-cultured TECs showed increased inflammation, apoptosis and oxidative stress following hypoxia/reoxygenation (H/R) injury. Disruption of TGF-βRII attenuated cell injury induced by H/R in HG-treated TECs. Consistently, Smad3 knockdown in diabetic kidney attenuated I/R-induced AKI. Mechanistically, Smad3 binds to p53 and enhances p53 activity in cells treated with HG and H/R, which may lead to TECs apoptosis. Additionally, ChIP assay showed that Smad3 bound with the promoter region of NOX4 and induced ROS production and inflammation. In conclusion, our results demonstrate that Smad3 promotes AKI susceptibility in diabetic mice by interacting with p53 and NOX4. Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

基金：
National Natural Science Foundation of China (No.81300580, 81570623 and 81970584), Science and Technological Fund of Anhui Province for Outstanding Youth of China (No.1608085J07) and by Open Funding of Key Lab of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Project #: KF201903.
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2019]版：
大类 | 1 区 生物
小类 | 2 区 生化与分子生物学
最新[2025]版：
大类 | 1 区 生物学
小类 | 1 区 生化与分子生物学
第一作者：
第一作者机构： [1]The Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, The Key Laboratory of Antiinflammatory and Immune Medicines, Ministry of Education, Hefei, 230032, China
共同第一作者：
通讯作者：
通讯机构： [1]The Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, The Key Laboratory of Antiinflammatory and Immune Medicines, Ministry of Education, Hefei, 230032, China [*1]School of Pharmacy, Anhui Medical University, Hefei, Anhui, 230032, China
推荐引用方式(GB/T 7714)：
Wang Jia-Nan,Yang Qin,Yang Chen,et al.Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production.[J].Redox biology.2020,32:101479.doi:10.1016/j.redox.2020.101479.
APA：
Wang Jia-Nan,Yang Qin,Yang Chen,Cai Yu-Ting,Xing Tian...&Meng Xiao-Ming.(2020).Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production..Redox biology,32,
MLA：
Wang Jia-Nan,et al."Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production.".Redox biology 32.(2020):101479

相关文献

[1]Silymarin nanoliposomes attenuate renal injury on diabetic nephropathy rats via co-suppressing TGF-β/Smad and JAK2/STAT3/SOCS1 pathway. [2]Artesunate-Nanoliposome-TPP, a Novel Drug Delivery System That Targets the Mitochondria, Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Oxidative Stress and Inflammatory Effects [3]endophilin A2抑制小鼠肾间质纤维化的形成 [4]Transforming growth factor-β signaling: From tissue fibrosis to therapeutic opportunities [5]Tanshinone IIA attenuates renal fibrosis and inflammation via altering expression of TGF-β/Smad and NF-κB signaling pathway in 5/6 nephrectomized rats. [6]Endophilin A2 protects against renal fibrosis by targeting TGF-β/Smad signaling [7]Arachidonic acid metabolism as a therapeutic target in AKI-to-CKD transition [8]Connexin32 promotes the activation of Foxo3a to ameliorate diabetic nephropathy via inhibiting the polyubiquitination and degradation of Sirt1 [9]Ginkgo biloba Extract 50 (GBE50) Exerts Antifibrotic and Antioxidant Effects on Pulmonary Fibrosis in Mice by Regulating Nrf2 and TGF-β1/Smad Pathways [10]Diverse Role of TGF-β in Kidney Disease

资源点击量：2020 今日访问量：0 总访问量：646 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