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浙江大学学报（医学版）
浙江大学学报（医学版）  2019, Vol. 48 Issue (2): 214-218    DOI: 10.3785/j.issn.1008-9292.2019.04.14
综述     
微小RNA-21在心脏疾病中的研究进展
杨坤(),胡晓晟*()
浙江大学医学院附属第一医院心血管内科, 浙江 杭州 310003
Research progress on miR-21 in heart diseases
YANG Kun(),HU Xiaosheng*()
Department of Cardiology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
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摘要：

心肌凋亡、心脏肥大、心肌纤维化和心房电重构等病理过程参与了绝大部分心脏疾病的发生和发展，阐明其中病理机制有助于心脏疾病的诊断和治疗。近年研究发现，微小RNA-21（miR-21）作为一类新型内源性调节因子，具有抑制心肌细胞凋亡、改善高血压和心脏肥大、促进心肌纤维化进展、促进心房电重构等作用。本文就miR-21在心脏疾病中的作用和机制研究进展进行综述，并初步探讨miRNA作为心脏疾病临床诊断标志物和治疗靶点的应用前景。
关键词： 微RNA;  基因表达;  心脏扩大;  肌细胞, 心脏;  细胞凋亡;  心脏病/治疗;  心脏病/诊断;  综述    
Abstract:

Pathological processes such as myocardial apoptosis, cardiac hypertrophy, myocardial fibrosis, and cardiac electrical remodeling are involved in the development and progression of most cardiac diseases. MicroRNA-21 (miR-21) has been found to play an important role in heart diseases as a novel type of endogenous regulators, which can inhibit cardiomyocyte apoptosis, improve hypertension and cardiac hypertrophy, promote myocardial fibrosis and atrial electrical remodeling. In this review, we summarize the research progress on the function of miR-21 in heart diseases and its mechanism, and discuss its potential application in diagnosis and treatment of heart diseases.
Key words: MicroRNAs    Gene expression    Cardiomegaly    Myocytes, cardiac    Apoptosis    Heart diseases/therapy    Heart diseases/diagnosis    Review
收稿日期: 2019-01-10 出版日期: 2019-07-24
CLC:  R363  
基金资助: 浙江省医药卫生科技计划(2018KY047)
通讯作者: 胡晓晟     E-mail: 21618023@zju.edu.cn;1196017@zju.edu.cn
作者简介: 杨坤(1993-), 男, 硕士研究生, 主要从事心肌纤维化研究; E-mail:21618023@zju.edu.cn; https://orcid.org/0000-0003-1786-3446
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杨坤,胡晓晟. 微小RNA-21在心脏疾病中的研究进展[J]. 浙江大学学报（医学版）, 2019, 48(2): 214-218.

YANG Kun,HU Xiaosheng. Research progress on miR-21 in heart diseases. J Zhejiang Univ (Med Sci), 2019, 48(2): 214-218.

链接本文:

http://www.zjujournals.com/med/CN/10.3785/j.issn.1008-9292.2019.04.14    或    http://www.zjujournals.com/med/CN/Y2019/V48/I2/214

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