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HCV-Induced Oxidative Stress: Battlefield-Winning Strategy
About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). The persistence of the infection is controlled by several mechanisms including the induction of oxidative stress. HCV relies on this strategy to redirect lipid metabolism machinery and escape immune response. T...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4880679/ https://www.ncbi.nlm.nih.gov/pubmed/27293514 http://dx.doi.org/10.1155/2016/7425628 |
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author | Rebbani, Khadija Tsukiyama-Kohara, Kyoko |
author_facet | Rebbani, Khadija Tsukiyama-Kohara, Kyoko |
author_sort | Rebbani, Khadija |
collection | PubMed |
description | About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). The persistence of the infection is controlled by several mechanisms including the induction of oxidative stress. HCV relies on this strategy to redirect lipid metabolism machinery and escape immune response. The 3β-hydroxysterol Δ24-reductase (DHCR24) is one of the newly discovered host markers of oxidative stress. This protein, as HCV-induced oxidative stress responsive protein, may play a critical role in the pathogenesis of HCV chronic infection and associated liver diseases, when aberrantly expressed. The sustained expression of DHCR24 in response to HCV-induced oxidative stress results in suppression of nuclear p53 activity by blocking its acetylation and increasing its interaction with MDM2 in the cytoplasm leading to its degradation, which may induce hepatocarcinogenesis. |
format | Online Article Text |
id | pubmed-4880679 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-48806792016-06-12 HCV-Induced Oxidative Stress: Battlefield-Winning Strategy Rebbani, Khadija Tsukiyama-Kohara, Kyoko Oxid Med Cell Longev Review Article About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). The persistence of the infection is controlled by several mechanisms including the induction of oxidative stress. HCV relies on this strategy to redirect lipid metabolism machinery and escape immune response. The 3β-hydroxysterol Δ24-reductase (DHCR24) is one of the newly discovered host markers of oxidative stress. This protein, as HCV-induced oxidative stress responsive protein, may play a critical role in the pathogenesis of HCV chronic infection and associated liver diseases, when aberrantly expressed. The sustained expression of DHCR24 in response to HCV-induced oxidative stress results in suppression of nuclear p53 activity by blocking its acetylation and increasing its interaction with MDM2 in the cytoplasm leading to its degradation, which may induce hepatocarcinogenesis. Hindawi Publishing Corporation 2016 2016-05-12 /pmc/articles/PMC4880679/ /pubmed/27293514 http://dx.doi.org/10.1155/2016/7425628 Text en Copyright © 2016 K. Rebbani and K. Tsukiyama-Kohara. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Rebbani, Khadija Tsukiyama-Kohara, Kyoko HCV-Induced Oxidative Stress: Battlefield-Winning Strategy |
title | HCV-Induced Oxidative Stress: Battlefield-Winning Strategy |
title_full | HCV-Induced Oxidative Stress: Battlefield-Winning Strategy |
title_fullStr | HCV-Induced Oxidative Stress: Battlefield-Winning Strategy |
title_full_unstemmed | HCV-Induced Oxidative Stress: Battlefield-Winning Strategy |
title_short | HCV-Induced Oxidative Stress: Battlefield-Winning Strategy |
title_sort | hcv-induced oxidative stress: battlefield-winning strategy |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4880679/ https://www.ncbi.nlm.nih.gov/pubmed/27293514 http://dx.doi.org/10.1155/2016/7425628 |
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