MicroRNA-93 elevation after myocardial infarction is cardiac protective
MicroRNA-93 elevation after myocardial infarction is cardiac protective
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DOI：
10.1016/j.mehy.2017.07.003
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发表时间：
2017-09-01
影响因子：
4.7
通讯作者：
Wang, Neng
中科院分区：
文献类型：
--
作者：
Li, Kai;Lin, Tao;Wang, Neng
冠状动脉疾病(CAD)是危害人类健康的最严重的疾病之一，心肌梗死(MI)是CAD的一种急性表现形式。心肌梗死治疗的最新进展显著降低了死亡率。然而，随之而来的慢性充血性心力衰竭和心室重构困扰着越来越多的MI患者。MicroRNAs(MiR)参与了心脏重构过程，最近的一项研究表明，在冠心病患者的血液中miR-93水平升高。与人类冠心病相似，我们发现miR-93在MI模型小鼠的脑室组织和血液中均升高，并且miR-93是由低氧培养的心肌细胞分泌的。有趣的是，miR-93抑制细胞凋亡，保护心肌细胞免受缺血/再灌注损伤。在中风和外周动脉疾病等其他类型的缺血性疾病中，miR-93通过促进血管生成、诱导巨噬细胞M2极化和抗氧化作用而显示出长期的保护作用。这些作用有利于抑制心肌梗死后的心室重构。在一项先导性实验中，我们指出，miR-93基因敲除会在小鼠心肌梗死后30天内恶化心脏重构。因此，我们推测MI后心肌细胞miR-93的上调和分泌是适应性的，可以抑制心脏重构和心力衰竭。(C)爱思唯尔有限公司发布的2017年。
Coronary Artery Disease (CAD) is one of the most serious diseases that endangers human health worldwide, myocardial infarction (MI) is an acute form of CAD. Recent developments in MI therapies have resulted in significant reductions in mortality. However, subsequent chronic congestive heart failure and ventricle remodeling plagues an increasing number of MI patients. MicroRNAs (miR) have been reported to be involved in the process of cardiac remodeling, a recent study shows that miR-93 is elevated in the blood of CAD patients. Similar to human CAD, we found miR-93 is elevated both in ventricle tissue and blood in mice MI model, and miR-93 is secreted from cardiomyocytes cultured under hypoxia. Interestingly, miR-93 inhibits apoptosis and protects cardiomyocytes from ischemia/reperfusion injury. In other type of ischemic disease like stoke and peripheral arterial disease, miR-93 shows long term protective effects via enhancing angiogenesis, inducing macrophage M2 polarization and antioxidant effects. These effects are favorable for ventricle remodeling inhibition after MI. In a pilot experiment, we indicated that miR-93 knockdown deteriorate cardiac remodeling in 30 days after MI in mice models. Therefore, we hypothesize that miR-93 upregulation and secretion from cardiomyocytes after MI is adaptive, which could inhibit cardiac remodeling and heart failure. (C) 2017 Published by Elsevier Ltd.