Hepatitis C virus‐induced oxidative stress and mitochondrial dysfunction: A focus on recent advances in proteomics
- 5 November 2010
- journal article
- review article
- Published by Wiley in Proteomics – Clinical Applications
- Vol. 4 (10-11), 782-793
- https://doi.org/10.1002/prca.201000049
Abstract
The natural history of chronic hepatitis C virus (HCV) infection presents two major aspects. On one side, the illness is by itself benign, whereas, on the other side, epidemiological evidence clearly identifies chronic HCV infection as the principal cause of cirrhosis, hepatocellular carcinoma, and extrahepatic diseases, such as autoimmune type II mixed cryoglobulinemia and some B cell non‐Hodgkin's lymphomas. The mechanisms responsible for the progression of liver disease to severe liver injury are still poorly understood. Nonetheless, considerable biological data and studies from animal models suggest that oxidative stress contributes to steatohepatitis and that the increased generation of reactive oxygen and nitrogen species, together with the decreased antioxidant defense, promotes the development of hepatic and extrahepatic complications of HCV infection. The principal mechanisms causing oxidative stress in HCV‐positive subjects have only been partially elucidated and have identified chronic inflammation, iron overload, ER stress, and a direct activity of HCV proteins in increasing mitochondrial ROS production, as key events. This review summarizes current knowledge regarding mechanisms of HCV‐induced oxidative stress with its long‐term effects in the context of HCV‐related diseases, and includes a discussion of recent contributions from proteomics studies.Keywords
Funding Information
- Programma Integrato Oncologia, Tematica 2 and “Associazione Italiana per la Ricerca sul Cancro”
This publication has 101 references indexed in Scilit:
- Hepatitis C Virus Regulates Transforming Growth Factor β1 Production Through the Generation of Reactive Oxygen Species in a Nuclear Factor κB–Dependent MannerGastroenterology, 2010
- Hepatocyte NAD(P)H oxidases as an endogenous source of reactive oxygen species during hepatitis C virus infectionHepatology, 2010
- Hepatitis C Virus Impairs p53 via Persistent Overexpression of 3β-Hydroxysterol Δ24-ReductaseJournal of Biological Chemistry, 2009
- Redox proteomics identification of 4‐hydroxynonenal‐modified brain proteins in Alzheimer's disease: Role of lipid peroxidation in Alzheimer's disease pathogenesisProteomics – Clinical Applications, 2009
- Detection of novel biomarkers of liver cirrhosis by proteomic analysisHepatology, 2008
- HCV inhibits antigen processing and presentation and induces oxidative stress response in gastric mucosaProteomics – Clinical Applications, 2008
- Hepatitis C Virus–Induced Reactive Oxygen Species Raise Hepatic Iron Level in Mice by Reducing Hepcidin TranscriptionGastroenterology, 2008
- Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virusNature, 2005
- Identification and Characterization of MAVS, a Mitochondrial Antiviral Signaling Protein that Activates NF-κB and IRF3Cell, 2005
- Structural biology of hepatitis C virusHepatology, 2004