[1]孙硕,毛露,史虓悦,等.内皮素-1促进慢性心功能衰竭进展机制研究[J].心血管病学进展,2019,(6):927-930.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.022]
 SUN Shuo,MAO Lu,SHI Xiaoyue,et al.Mechanism of Endothelin-1 in Promoting Progression of Chronic Heart Failure[J].Advances in Cardiovascular Diseases,2019,(6):927-930.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.022]
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2019年6期
页码:
927-930
栏目:
综述
出版日期:
2019-09-25

文章信息/Info

Title:
Mechanism of Endothelin-1 in Promoting Progression of Chronic Heart Failure
作者:
孙硕1毛露2史虓悦1Dirk Hermann3 陈艾东13 *
(1.心血管病靶向干预重点实验室 南京医科大学,江苏 南京 211166;2.东南大学附属中大医院 东南大学,江苏 南京 21 0096;3.神经生物学研究中心 杜伊斯堡-埃森大学,德国 埃森 45122)
Author(s):
SUN Shuo 1 MAO Lu 2 SHI Xiaoyue1 Dirk Hermann3 CHEN Aidong 13
(1.Key Laboratory of Targeting Interventions for Cardiovascular Diseases, Nanjing Medical University, Nanjing 211166,Jiangsu, China; 2.Zhongda Hospital Affiliated to Southeast University, Southeast University, Nanjing 210096,Jiangsu, China; 3.Center for Neurobiology, Duisburg -Essen University, Essen 45122, Germany)?
Funded by: National Natural Science Foundation of China (31571168) National Public Fund for Study Abroad (20173059)
Keywords:
Endothelin-1 Chronic heart failure Receptor antagonist
DOI:
10.16806/j.cnki.issn.1004-3934.2019.06.022
摘要:

内皮素-1是一种21个氨基酸的肽,为目前发现的最强的血管收缩和升压物。慢性心功能衰竭时,内皮素-1浓度升高,其对心肌细胞具有直接毒性、强烈的正性肌力作用、致使心肌细胞肥大活性和诱导室性心律失常等效应,参与慢性心功能衰竭的恶化进展。内皮素-1通过激活两种受体亚型内皮素-1A和内皮素-1B受体起作用,这两种受体亚型根据细胞类型与各种GTP结合蛋白偶联,发挥相应的生物学效应。内皮素-1拮抗剂有望成为慢性心功能衰竭治疗新靶点。现就内皮素-1促进慢性心功能衰竭进展机制做一综合阐述,旨在为本病的治疗梳理出新的治疗靶点。

Abstract:
Endothelin-1 (ET-1) is a 21 amino acid peptide that is the strongest vasoconstrictor and booster pressor substance found so far. In chronic heart failure, the concentration of ET-1 increased, which is directly toxic to cardiomyocytes, and causes strong positive inotropic effects. It can cause cardiomyocyte hypertrophy,induce ventricular arrhythmia,and participate in chronic cardiac dysfunction. ET-1 acts by activating two receptor subtypes, ET A and ET B receptors, which are conjugated to various GTP-binding proteins depending on the cell type, exerting corresponding biological effects. ET-1 antagonists are expected to become new drug targets for the treatment of chronic heart failure. In this paper, a comprehensive review on the progress of ET-1 in promoting the progression of chronic heart failure is aimed at combing a new therapeutic target for the treatment of this disease.

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备注/Memo

备注/Memo:
通讯作者:陈艾东,E-mail:aidongchen@njmu.edu.cn?收稿日期:2019-03-12
基金项目: 国家自然科学基金面上项目( 31571168,30870908,81571246);国家公派留学基金(20173059)
更新日期/Last Update: 2019-12-17