IMR Press / FBS / Volume 15 / Issue 3 / DOI: 10.31083/j.fbs1503010
Open Access Review
The Role of Mitochondrial Dysfunction in the Development of Acute and Chronic Hepatitis С
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1 Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia
2 Laboratory of Cellular and Molecular Pathology of the Cardiovascular System, Petrovsky National Research Centre of Surgery, 119991 Moscow, Russia
3 Department of Cardiac Surgery, Moscow Regional Research and Clinical Institute (MONIKI), 129110 Moscow, Russia
*Correspondence: (Alexander Blagov); (Alexander Orekhov)
These authors contributed equally.
Front. Biosci. (Schol Ed) 2023, 15(3), 10;
Submitted: 26 May 2023 | Revised: 5 September 2023 | Accepted: 19 September 2023 | Published: 24 September 2023
Copyright: © 2023 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

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.

hepatitis C
mitochondrial dysfunction
reactive oxygen species
Grant # 23-65-10014/Russian Science Foundation
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