Nox4-dependent ROS production is involved in CVB3-induced myocardial apoptosis

Nox4-dependent ROS production is involved in CVB3-induced myocardial apoptosis
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Nox4 依赖性 ROS 产生参与 CVB3 诱导的心肌细胞凋亡

DOI:
10.1016/j.bbrc.2018.07.093
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发表时间:
2018-09-10
影响因子:
3.1
通讯作者:
Zhao, Dechao
Zhao, Dechao
中科院分区:
生物学4区
文献类型:
--
作者:
Chi, Jinyu;Yu, Shouxian;Zhao, Dechao

文献摘要

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病毒性心肌炎是一种严重影响人体健康的心血管疾病。其机制尚不清楚。柯萨奇病毒B3 (CVB3)是小核糖核酸病毒家族的一员,是病毒性心肌炎的主要病因。我们组在CVB3病毒感染小鼠模型中检测了这些基因,证实NADPH氧化酶基因在感染急性期有高表达的趋势。NADPH氧化酶的同源物Nox4是否参与病毒性心肌炎的发生过程尚未见报道。在本研究中,我们发现Nox4在体内和体外的病毒性心肌炎中表达增加。DPI是Nox4的非特异性抑制剂,体内注射后可改善cvb3诱导的心肌炎。DPI还能抑制细胞内ROS释放和细胞凋亡。我们的数据表明,nox4依赖性ROS的产生参与了cvb3诱导的心肌凋亡。(C) 2018爱思唯尔公司版权所有。
Viral myocarditis is a cardiovascular disease that seriously affects human health. Its mechanism is not clear. Coxsackievirus B3 (CVB3) is a member of the picornavirus family and is the leading cause of viral myocarditis. Our group tested the genes in a mouse model of CVB3 virus infection and confirmed that the NADPH oxidase gene had a high expression trend in the acute phase of infection. Whether Nox4, the homologue of NADPH oxidase, participates in the process of viral myocarditis has not been reported. In this study, we found increased expression of Nox4 in viral myocarditis in vivo and in vitro. DPI is a nonspecific inhibitor of Nox4 that improved CVB3-induced myocarditis after injection in vivo. DPI also inhibited intracellular ROS release and apoptosis in vitro. Our data indicated that Nox4-dependent ROS production was involved in CVB3-induced myocardial apoptosis. (C) 2018 Elsevier Inc. All rights reserved.