The Role of Mitochondrial Dysfunction in the Development of Acute and Chronic Hepatitis С.

Alexander Blagov, Vasily Sukhorukov, Varvara Orekhova, Anton Postnov, Mikhail Popov, Alexander Orekhov
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Abstract

Currently, the issue relating to the discussion raised in this article appears to be for what purposes the hepatitis C virus (HCV) modulates cellular processes, such as antiviral defense, metabolism, apoptosis, and mitochondrial dynamics, by inhibiting the activity or expression of mitochondrial proteins and a number of cellular proteins. Additionally, to what pathological changes do these alterations lead? Thus, the aim of this review is to propose potential protein mitochondrial targets of HCV for the future development of new drugs aimed at inhibiting its interaction with cellular proteins. Considering current analyses in the literature, promising targets for the acute and chronic phases of HCV are proposed which include mitochondrial antiviral signaling (MAVS) (antiviral response protein), Parkin (mitophagy protein), Drp1 (mitochondrial fission protein), subunits 1 and 4 of the electron transport chain (ETC) complex (oxidative phosphorylation proteins), among others. This review illustrates how viral strategies for modulating cellular processes involving HCV proteins differ in the acute and chronic phases and, as a result, the complications that arise.

线粒体功能障碍在急慢性丙型肝炎发展中的作用。
目前,与本文中提出的讨论有关的问题似乎是,丙型肝炎病毒(HCV)通过抑制线粒体蛋白和许多细胞蛋白的活性或表达来调节细胞过程,如抗病毒防御、代谢、细胞凋亡和线粒体动力学。此外,这些改变会导致什么样的病理变化?因此,本综述的目的是为未来开发旨在抑制其与细胞蛋白相互作用的新药提出HCV的潜在蛋白质线粒体靶点。考虑到目前文献中的分析,提出了丙型肝炎急性期和慢性期的有希望的靶点,包括线粒体抗病毒信号传导(MAVS)(抗病毒反应蛋白)、Parkin(线粒体自噬蛋白)、Drp1(线粒体分裂蛋白)、电子输运链(ETC)复合物的亚基1和4(氧化磷酸化蛋白)等。这篇综述说明了病毒在急性期和慢性期调节涉及HCV蛋白的细胞过程的策略是如何不同的,因此也说明了出现的并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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