中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
首页 机构 成果 学者
  
  1. CAS IR Grid
  2. 上海营养与健康研究所
  3. 中国科学院上海生命科学研究院营养科学研究所
Suppression of Endothelial-to-Mesenchymal Transition by SIRT (Sirtuin) 3 Alleviated the Development of Hypertensive Renal Injury

文献类型：期刊论文

作者Lin, Jing-rong3,4; Zhang, Ze-bei3,4; Shen, Wei-li3,4; Li, Xiao-dong3,4; Wei, Tong3,4; Ruan, Cheng-chao3,4; Zhu, Ding-liang3,4; Gao, Ping-jin1,2,3,4; Zheng, Yan-jun1,2; Chen, Xiao-hui1,2
刊名HYPERTENSION
出版日期2018
卷号72期号:2页码:350-360
关键词angiotensin II EndoMT reactive oxygen species renal injury SIRT3
ISSN号0194-911X
DOI10.1161/HYPERTENSIONAHA.118.10482
文献子类Article
英文摘要Endothelial-to-mesenchymal transition (EndoMT) has recently emerged as a potentially important contributor in promoting fibrosis in chronic kidney disease. However, little is known about the role and molecular basis of its involvement in hypertensive renal injury. Here, we aim to determine the role of SIRT (sirtuin) 3 on EndoMT in hypertensive renal injury and to explore its underlying mechanisms. We found that SIRT3 expression was significantly reduced in Ang II (angiotensin II)-induced hypertensive model, accompanied with induction of EndoMT and increased reactive oxygen species and renal fibrosis. In SIRT3(-/-) (SIRT3 knockout) mice subjected to Ang II infusion, renal dysfunction was aggravated with an increased EndoMT and reactive oxygen species level, whereas in SIRT3-Tg(EC) (SIRT3 endothelial cell-specific transgenic) mice, the Ang II-induced renal fibrosis and EndoMT and oxidative stress were ameliorated. With primary mouse glomerular endothelial cells, we confirmed that Ang II treatment initiated EndoMT and decreased catalase expression, which were suppressed by SIRT3 overexpression. Using immunoprecipitation, luciferase, and chromatin immunoprecipitation assay, we demonstrated that SIRT3-mediated deacetylation and nuclear localization of Foxo3a (forkhead box O3a) resulted in activated Foxo3a-dependent catalase expression. Moreover, Foxo3a knockdown abolished SIRT3-mediated suppression of EndoMT. In conclusion, these results established the SIRT3-Foxo3a-catalase pathway as a critical factor in the maintenance of endothelial homeostasis and point to an important role of EndoMT in the vascular pathology of renal fibrosis, which may provide a new therapeutic target to impede the progression of hypertensive renal injury.
学科主题Cardiovascular System & Cardiology
WOS关键词PULMONARY ARTERIAL-HYPERTENSION ; OXIDATIVE STRESS ; KIDNEY FIBROSIS ; ANGIOTENSIN-II ; MITOCHONDRIAL-FUNCTION ; CARDIAC FIBROSIS ; DISEASE ; MICE ; CONTRIBUTES ; DAMAGE
语种英语
WOS记录号WOS:000438231100021
出版者LIPPINCOTT WILLIAMS & WILKINS
版本出版稿
源URL[http://202.127.25.144/handle/331004/554]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Lab Vasc Biol, Beijing, Peoples R China;
2.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Beijing, Peoples R China,
3.Shanghai Jiao Tong Univ, State Key Lab Med Genom, Shanghai Key Lab Hypertens,Dept Hypertens, Ruijin Hosp,Sch Med, Shanghai, Peoples R China;
4.Shanghai Res Inst Hypertens, Shanghai, Peoples R China;
推荐引用方式
GB/T 7714		 Lin, Jing-rong,Zhang, Ze-bei,Shen, Wei-li,et al. Suppression of Endothelial-to-Mesenchymal Transition by SIRT (Sirtuin) 3 Alleviated the Development of Hypertensive Renal Injury[J]. HYPERTENSION,2018,72(2):350-360.
APA Lin, Jing-rong.,Zhang, Ze-bei.,Shen, Wei-li.,Li, Xiao-dong.,Wei, Tong.,...&,.(2018).Suppression of Endothelial-to-Mesenchymal Transition by SIRT (Sirtuin) 3 Alleviated the Development of Hypertensive Renal Injury.HYPERTENSION,72(2),350-360.
MLA Lin, Jing-rong,et al."Suppression of Endothelial-to-Mesenchymal Transition by SIRT (Sirtuin) 3 Alleviated the Development of Hypertensive Renal Injury".HYPERTENSION 72.2(2018):350-360.

入库方式： OAI收割

来源：上海营养与健康研究所

浏览0
下载0
收藏0
其他版本

除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。