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学科主题: 临床医学
题名:
Trimetazidine inhibits pressure overload-induced cardiac fibrosis through NADPH oxidase-ROS-CTGF pathway
作者: Liu, Xuehui1,2; Gai, Yingli1,2,3; Liu, Fei1,2; Gao, Wei1,2; Zhang, Youyi1,2; Xu, Ming1,2; Li, Zhaoping1,2
关键词: Trimetazidine ; Cardiac fibrosis ; Connective tissue growth factor ; Reactive oxygen species ; NADPH oxidase
刊名: CARDIOVASCULAR RESEARCH
发表日期: 2010-10-01
DOI: 10.1093/cvr/cvq181
卷: 88, 期:1, 页:150-158
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems
研究领域[WOS]: Cardiovascular System & Cardiology
关键词[WOS]: TISSUE GROWTH-FACTOR ; ISCHEMIA-REPERFUSION INJURY ; LEFT-VENTRICULAR FUNCTION ; CHRONIC HEART-FAILURE ; FATTY-ACID OXIDATION ; ANGIOTENSIN-II ; MYOCARDIAL FIBROSIS ; SIGNALING PATHWAYS ; HYPERTROPHY ; CARDIOMYOPATHY
英文摘要:

Cardiac fibrosis contributes to the transition from compensated ventricular hypertrophy to heart failure, which can be promoted by connective tissue growth factor (CTGF). Trimetazidine (TMZ), an anti-angina drug, also has benefits in non-ischaemic heart disease. We wondered whether TMZ has an effect on cardiac fibrosis from pressure overload by downregulating CTGF.

Male Sprague-Dawley rats underwent transverse aortic constriction (TAC) or sham operation and then after 20 weeks were assigned to receive TMZ or saline for another 5 weeks. TMZ significantly inhibited collagen accumulation, CTGF expression, and reactive oxygen species (ROS) production induced by TAC. Furthermore, the effects of TMZ on ROS, the upstream signal of CTGF synthesis signal transduction, were evaluated in cardiac fibroblasts. The result showed that the ROS level was reduced by TMZ on stimulation with angiotensin II. Additionally, the NADPH oxidase activity was ameliorated with TMZ by the regulation of translocation of its subunit Rac1.

TMZ effectively inhibits myocardial fibrosis, perhaps through the NADPH oxidase-ROS-CTGF signalling pathway. Our findings may be used to provide new clues for the potential function of TMZ in pressure overload-induced myocardial fibrosis.

语种: 英语
所属项目编号: 2006CB503806 ; 2007CB512107 ; 30821001 ; 2007AA02Z457 ; 7082101
项目资助者: National Key Basic Research Program (NKBRP) of the People&prime ; s Republic of China ; Natural Science Foundation of China ; 863 Program ; University and Beijing Talents Foundation ; Natural Science Foundation of Beijing
WOS记录号: WOS:000281714600019
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/58033
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Peking Univ, Dept Cardiol, Inst Vasc Med, Hosp 3, Beijing 100191, Peoples R China
2.Peking Univ, Key Lab Mol Cardiovasc Sci, Minist Educ, Beijing 100191, Peoples R China
3.Beijing Univ Aeronaut & Astronaut, Hosp Beijing Univ Aeronaut & Astronaut, Beijing 100191, Peoples R China

Recommended Citation:
Liu, Xuehui,Gai, Yingli,Liu, Fei,et al. Trimetazidine inhibits pressure overload-induced cardiac fibrosis through NADPH oxidase-ROS-CTGF pathway[J]. CARDIOVASCULAR RESEARCH,2010,88(1):150-158.
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