Nerve growth factor-induced Akt/mTOR activation protects the ischemic heart via restoring autophagic flux and attenuating ubiquitinated protein accumulation

doi:10.18632/oncotarget.14284

科研成果详情

题名	Nerve growth factor-induced Akt/mTOR activation protects the ischemic heart via restoring autophagic flux and attenuating ubiquitinated protein accumulation
作者	Wang, Zhou-Guang 1,2,3; Li, Hao1; Huang, Yan 2; Li, Rui 2; Wang, Xiao-Fan2; Yu, Li-Xia 2; Guang, Xue-Qiang 1; Li, Lei 1; Zhang, Hong-Yu2; Zhao, Ying-Zheng2; Zhang, Chunxiang1; Li, Xiao-Kun2,3; Wu, Rong-Zhou1; Chu, Mao-Ping1; Xiao, Jian1,2
发表日期	2017-01-17
发表期刊	ONCOTARGET 影响因子和分区
语种	英语
原始文献类型	Article
关键词	NGF myocardial ischemia/reperfusion autophagy PI3K/Akt/mTOR ubiquitin
其他关键词	MYOCARDIAL ISCHEMIA/REPERFUSION INJURY ; ENDOPLASMIC-RETICULUM STRESS ; REGULATES AUTOPHAGY ; PROTEASOME SYSTEM ; C-KIT ; DISEASE ; REPERFUSION ; PATHWAY ; ISCHAEMIA/REPERFUSION ; INFARCTION
摘要	The dysregulation of autophagy is related to a variety of cardiovascular diseases, such as myocardial ischemia/reperfusion (I/R). Nerve growth factor (NGF) has been shown to have therapeutic potential in ischaemic heart injury. In this study, we demonstrate that NGF administration can accelerate autophagic flux and attenuate protein ubiquitination in myocardial I/R heart. Our results showed that NGF could restored heart function and decreased the apoptosis of cardiomyocytes which induced by myocardial I/R injury. The protective effect of NGF is associated with the inhibition of autophagy related proteins. On another hand, NGF enhances the clearance of ubiquitinated protein and increases the survival of myocardial cell in vivo and in vitro. Additionally, NGF could activate the PI3K/AKT and mTOR signaling pathways. These results suggested that the cardioprotective effect of NGF is related to the restoration of autophagic flux and attenuation of protein ubiquitination via the activation of PI3K/AKT and mTOR pathway.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81372112, 81302775]; Zhejiang Provincial Program for the Cultivation of High-level Innovative Health talents; Science and technology project of Zhejiang Province [LY17H090017]
出版者	IMPACT JOURNALS LLC
出版地	ORCHARD PARK
ISSN	1949-2553
EISSN	1949-2553
卷号	8 期号:3 页码:5400-5413
DOI	10.18632/oncotarget.14284
页数	14
WOS类目	Oncology ; Cell Biology
WOS研究方向	Oncology ; Cell Biology
WOS记录号	WOS:000393228400132
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	28036273
PMC记录号	PMC5354918
SCOPUSEID	2-s2.0-85011954149
通讯作者地址	[Xiao, Jian]Institute of Cardiovascular Development and Translational Medicine,Children's Heart Center,The Second Affiliated Hospital,Wenzhou Medical University,Wenzhou,325027,China
Scopus学科分类	Oncology
引用统计	被引频次：29[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/18330
专题	附属第二医院药学院（分析测试中心）_分子药理研究与教学中心
通讯作者	Xiao, Jian
作者单位	1.Institute of Cardiovascular Development and Translational Medicine,Children's Heart Center,The Second Affiliated Hospital,Wenzhou Medical University,Wenzhou,325027,China; 2.Molecular Pharmacology Research Center,School of Pharmacy,Key Laboratory of Biotechnology and Pharmaceutical Engineering,Wenzhou Medical University,Wenzhou,325035,China; 3.Department of Biochemistry and Molecular Biology,College of Basic Medical Science,Jilin University,Changchun,130012,China
第一作者单位	附属第二医院; 药学院（分析测试中心）_分子药理研究与教学中心
通讯作者单位	附属第二医院
第一作者的第一单位	附属第二医院
推荐引用方式 GB/T 7714	Wang, Zhou-Guang,Li, Hao,Huang, Yan,et al. Nerve growth factor-induced Akt/mTOR activation protects the ischemic heart via restoring autophagic flux and attenuating ubiquitinated protein accumulation[J]. ONCOTARGET,2017,8(3):5400-5413.
APA	Wang, Zhou-Guang., Li, Hao., Huang, Yan., Li, Rui., Wang, Xiao-Fan., ... & Xiao, Jian. (2017). Nerve growth factor-induced Akt/mTOR activation protects the ischemic heart via restoring autophagic flux and attenuating ubiquitinated protein accumulation. ONCOTARGET, 8(3), 5400-5413.
MLA	Wang, Zhou-Guang,et al."Nerve growth factor-induced Akt/mTOR activation protects the ischemic heart via restoring autophagic flux and attenuating ubiquitinated protein accumulation".ONCOTARGET 8.3(2017):5400-5413.