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中华细胞与干细胞杂志(电子版) ›› 2019, Vol. 09 ›› Issue (06) : 363 -368. doi: 10.3877/cma.j.issn.2095-1221.2019.06.008

所属专题： 文献；

综述

miRNA在心肌梗死中的作用及其机制研究进展
曹润峰1, 沈立1,†()   
  1. 1. 200062　上海交通大学附属儿童医院　上海市儿童医院心胸外科
  • 收稿日期:2019-08-18 出版日期:2019-12-01
  • 通信作者: 沈立
  • 基金资助:
    国家自然科学基金资助项目(81371449)

Advances in the role of miRNAs in myocardial infarction and its mechanisms

Runfeng Cao1, Li Shen1,†()   

  1. 1. Department of Cardiothoracic Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai 200062, China
  • Received:2019-08-18 Published:2019-12-01
  • Corresponding author: Li Shen
  • About author:
    Corresponding author: Shen Li, Email:
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引用本文：

曹润峰, 沈立. miRNA在心肌梗死中的作用及其机制研究进展[J]. 中华细胞与干细胞杂志(电子版), 2019, 09(06): 363-368.

Runfeng Cao, Li Shen. Advances in the role of miRNAs in myocardial infarction and its mechanisms[J]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2019, 09(06): 363-368.

急性心肌梗死（AMI）是最常见的心血管事件，具有高发病率和高死亡率，严重威胁人类生命健康。微小RNA（miRNA）通过调节心肌细胞炎症、纤维化、细胞自噬及新生血管形成的表型机制发挥功能。本综述探讨了心肌梗死后miRNA上调及下调的分子机制，以及miRNA对心肌梗死早期诊断中的价值。

关键词: miRNA, 心肌梗死, 早期诊断, 分子机制, 外泌体

Acute myocardial infarction (AMI) is the most common cardiovascular event with high morbidity and mortality, which is a serious threat to human health. MicroRNAs (miRNAs) act as an important role by regulating cardiomyocyte inflammatory and fibrosis, regulation of autophagy and neovascularization. Here, we review the molecular mechanisms of up-regulation and down-regulation of miRNA after myocardial infarction and the early diagnostic value of miRNA for myocardial infarction

Key words: MicroRNA, Biomarkers for diagnosis, Myocardial infarction, Molecular mechanism, Exosomes
表1 血清miRNA在心肌梗死早期诊断的临床研究
miRNA 临床研究样本分析 引文
AMI样本数 对照组样本数
miR-22-5p，miR-132-5p，miR-150-3p 35 55 [9]
miR-26a-1，miR-146a和miR-199a-1 31 27 [10]
miR-17-5p，miR-126-5p，miR-145-3p 29 21 [11]
miR-150 59 59 [12]
miRNA-4478 80 80 [13]
miRNA-302b 76 30 [14]
miRNA-133a 102 110 [15]
miR-208b 100 80 [16]
miR-221-3p 27 16 [17]
表2 心梗时上调而起保护作用的miRNA及其分子机制
miRNA 研究对象 信号通路及靶点 作用细胞 效应机制 引文
miR-21 小鼠 TGF-β/ Smad7信号通路 心脏成纤维细胞 抑制心脏纤维化 [20]
miR-23a 小鼠 锰超氧化物歧化酶（MnSOD） 心肌细胞 抑制心肌凋亡 [21]
miR-92a 小鼠 自噬及代谢相关基因 内皮细胞
心肌细胞		 抑制自噬，调节代谢 [22]
miR-125b
miR-125b-5p		 小鼠 抑制促凋亡基因p53和BAK1及调节p53-Bnip3信号传导，抑制bak1和klf13基因 心肌细胞 抑制心肌细胞凋亡 [23,24]
[25]
miR-132 小鼠 调节Akt / eNOS / Bcl-2信号传导途径，抑制Ras-GTP酶活化蛋白和甲基-CpG结合蛋白2 内皮细胞 促进血管形成 [26]
miR-146b 小鼠 靶向Notch1 心肌细胞 抗凋亡及抑制炎症反应 [27]
miR-199a 小鼠 靶向GSK3β / mTOR信号传导及抑制Atg5 心肌细胞 抑制自噬及心肌肥大 [28]
miR-499 大鼠H9c2细胞 靶向SOX6,上调Bcl-2水平及下调Bax和caspase-3的表达水平 心肌细胞 抑制凋亡 [29]
miR-133a 大鼠 调节TGF-β1，Caspase9和Caspase3 心肌细胞
成纤维细胞		 抑制凋亡抑制心肌纤维化 [30]
miR-144 miR-451 小鼠 靶向调节CUGBP2-COX-2 心肌细胞 抑制心肌凋亡 [31]
miR-138 先心病心肌样本+ H9C2细胞 靶向MLK3/JNK /c-jun通路 心肌细胞 抑制心肌凋亡 [32]
miR-874 小鼠 靶向STAT3-JAK2 / STAT3信号传导途径 心肌细胞 抑制心肌凋亡 [33]
miR-26a 大鼠 调节Wnt信号通路，抑制GSK3β表达和促进Cx43表达 心肌细胞 降低心肌细胞的损伤 [34]
miR-210 小鼠 增加中性鞘磷脂酶2（nSMase2）的表达 心肌细胞心脏内皮细胞、成纤维细胞 抑制凋亡，增加新生血管密度，抑制心脏纤维化 [35]
miR-19a 大鼠 靶向PTEN的表达，激活Akt / ERK信号传导途径 心肌细胞 减少心肌细胞凋亡和维持线粒体膜电位 [36]
miR-126 缺血性心肌病裸鼠 促进HGF，TIMP-1/TIMP-2的表达 内皮细胞 促进新生血管形成，降低炎症反应 [37]
miR-21 小鼠 靶向抑制PDCD4 心肌细胞 抑制心肌细胞自噬 [38]
miR-126 小鼠 抑制Spred-1的表达来增强VEGF和FGF的促血管生成 内皮细胞 诱导内皮细胞的微血管形成和迁移 [39]
miR-214 心梗患者血清 抑制PUMA，PTEN，Bax和caspase 7基因的表达 心肌细胞 抑制心肌细胞的凋亡 [40]
miR-208b 大鼠 抑制GATA4 心脏成纤维细胞 抑制心肌纤维化 [41]
miR-211 大鼠 STAT3 / miR-211 / STAT5A信号传导 间充质干细胞 降低MI后不良重建 [42]
miR-206 大鼠 靶向Pim-1激酶 间充质干细胞 刺激细胞循环并增强体内心脏再生 [43]
miR-532 小鼠 调节miR-532-prss23轴 内皮-间质转化（EndMT） 减少EndMT，增加内皮细胞增值及新生血管的密度 [44]
表3 心梗时下调而起保护作用的miRNA及其分子机制
miRNA 研究对象 信号通路及靶点 作用细胞 效应机制 引文
miR-320 大鼠 靶向ASK1-JNK / p38通路，抑制IGF-1 心肌细胞 抑制凋亡 [45]
miR-181b 大鼠 靶向AKT3和PI3KR3 心肌细胞 抑制凋亡 [46]
miR-22 大鼠H9c2细胞 调节PI3K / AKT和JAK1 / STAT3途径。 心肌细胞 抗凋亡及抑制心肌纤维化 [47]
miR-20a 大鼠 靶向调节促凋亡因子Egln3/PHD3 心肌细胞 抑制心肌细胞凋亡 [48]
miR-320 小鼠 靶向热休克蛋白20 心肌细胞 抑制心肌细胞凋亡 [49]
miR-140 小鼠 靶向线粒体蛋白1 （Mfn1） 心肌细胞 抑制心肌细胞凋亡 [50]
miR-92a 心梗患者血清 抑制PUMA，PTEN，Bax及caspase 7表达 心肌细胞
内皮细胞		 促血管生成作用及抗炎症反应 [51]
miR-181a HEK293细胞，成肌L6细胞和H9c2细胞 靶向谷胱甘肽过氧化物酶-1 （GPx1） 心肌细胞内线粒体 抑制线粒体凋亡 [52]
miR-122 Pax-8基因敲除小鼠 调节CCK-8的表达和Caspase-3的活性 心肌细胞 抑制心肌细胞凋亡 [53]
miR-150 大鼠 靶向c-myb基因 心肌细胞 抑制心肌细胞凋亡 [54]
miR-375 小鼠 调节3-磷酸肌醇依赖性蛋白激酶-1（PDK-1）的表达及激活PDK-1介导的PI3/ AKT信号传导的 骨髓衍生祖细胞 增强BMPAC增殖和形成并抑制细胞凋亡 [55]
表4 心梗时上调而起伤害作用的miRNA及其分子机制
miRNA 研究对象 信号通路及靶点 作用细胞 效应机制 引文
miR-328 小鼠 激活TGF-β1途径 成纤维细胞 促进心肌纤维化 [57]
miR-98 大鼠 负调节Fas和caspase-3凋亡信号通路 心肌细胞 诱导心肌细胞凋亡 [58]
miR-34a 大鼠 负调节醛脱氢酶2 （ALDH2） 心肌细胞 诱导心肌细胞凋亡 [59]
miR-1 大鼠 沉默MAPK3基因及阻断PI3K / Akt途径 心肌细胞 增加心肌细胞的凋亡 [60]
miR-20 小鼠 靶向KATP亚基Kir6.1 心肌细胞 加速心肌细胞凋亡 [61]
miR-15b 大鼠 靶向腺嘌呤核苷酸转运蛋白1的ADP-核糖基化因子2（Ar12） 心肌细胞 降低线粒体完整性 [62]
miR-195 小鼠 靶向抑制Sirt1表达及Bcl-2的过表达 心肌细胞 诱导心肌细胞凋亡 [63]
miR -34a 小鼠 靶向PNUTS及Smad4. 心肌细胞 促进心脏纤维化，减少血管生成 [64]
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