miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase.
miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase.
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miR-23a 通过靶向锰超氧化物歧化酶调节心肌细胞凋亡
DOI：
10.14348/molcells.2017.0012
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发表时间：
2017-08
影响因子：
3.8
通讯作者：
Zhang YH
中科院分区：
文献类型：
--
作者：
Long B;Gan TY;Zhang RC;Zhang YH
心肌细胞凋亡是由各种细胞损伤引发的，心肌细胞凋亡的累积导致心力衰竭的发病机制。过量的活性氧（ROS）引起凋亡级联反应。锰超氧化物歧化酶（MnSOD）是一种重要的抗氧化酶，可将细胞内的活性氧转化为无害的产物。在这项研究中，我们表明，MnSOD下调过氧化氢处理或缺血/再灌注（I/R）损伤。MnSOD增强表达减轻I/R损伤诱导的心肌细胞凋亡和心肌梗死此外，我们发现miR-23 a直接调节MnSOD的表达。miR-23 a通过抑制MnSOD表达调控心肌细胞凋亡我们的研究揭示了一种由miR-23 a和MnSOD组成的调节心肌细胞凋亡的新模型。本研究为治疗凋亡相关的心脏疾病提供了新的思路。
Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. Excessive reactive oxygen species (ROS) provoke apoptotic cascades. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products. In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Enhanced expression of MnSOD attenuates cardiomyocyte apoptosis and myocardial infarction induced by I/R injury. Further, we show that miR-23a directly regulates the expression of MnSOD. miR-23a regulates cardiomyocyte apoptosis by suppressing the expression of MnSOD. Our study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. Our study provides a new method to tackling apoptosis related cardiac diseases.