期刊
VIRUSES-BASEL
卷 5, 期 2, 页码 439-469出版社
MDPI
DOI: 10.3390/v5020439
关键词
hepatitis C; oxidative stress; Nrf2/ARE pathway; antioxidant defense; iron homeostasis; regulation
类别
资金
- Russian Ministry of Education and Science [11.519.11.2017]
- Russian Foundation for Basic Research [10-04-00047a, 11-04-01569a, 12-04-90447-Ukr_a]
- Molecular and Cellular Biology Program of Presidium of Russian Academy of Sciences
- President of Russian Federation [MK-5035.2011.4]
- Swedish Research Council [K2009-66X-21053-01-3, K2011-79X-21744-01-6]
- New Visby program of the Swedish Institute [00747/2010, 00885/2011]
- ANRS
- Region Rhone Alpes
- Labex DevWeCan
- ANR
Hepatitis C virus (HCV) is the etiological agent accounting for chronic liver disease in approximately 2-3% of the population worldwide. HCV infection often leads to liver fibrosis and cirrhosis, various metabolic alterations including steatosis, insulin and interferon resistance or iron overload, and development of hepatocellular carcinoma or non-Hodgkin lymphoma. Multiple molecular mechanisms that trigger the emergence and development of each of these pathogenic processes have been identified so far. One of these involves marked induction of a reactive oxygen species (ROS) in infected cells leading to oxidative stress. To date, markers of oxidative stress were observed both in chronic hepatitis C patients and in various in vitro systems, including replicons or stable cell lines expressing viral proteins. The search for ROS sources in HCV-infected cells revealed several mechanisms of ROS production and thus a number of cellular proteins have become targets for future studies. Furthermore, during last several years it has been shown that HCV modifies antioxidant defense mechanisms. The aim of this review is to summarize the present state of art in the field and to try to predict directions for future studies.
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