Hepatitis C Virus Infection: Molecular Pathways to Steatosis, Insulin Resistance and Oxidative Stress

被引：42

作者：

Clement, Sophie ^{[1
]}

Pascarella, Stephanie ^{[1
]}

Negro, Francesco ^{[1
,2
]}

机构：

[1] Univ Hosp, Div Clin Pathol, Geneva, Switzerland

[2] Univ Hosp, Div Gastroenterol & Hepatol, Geneva, Switzerland

来源：

VIRUSES-BASEL | 2009年 / 1卷 / 02期

基金：

瑞士国家科学基金会;

关键词：

hepatitis C; reactive oxygen species; insulin signaling; lipid accumulation; TRIGLYCERIDE TRANSFER PROTEIN; FATTY-ACID SYNTHASE; PEGINTERFERON PLUS RIBAVIRIN; GENOTYPE-SPECIFIC MECHANISMS; ACTIVATED-RECEPTOR-ALPHA; CORE PROTEIN; ANTIVIRAL THERAPY; VIRAL-HEPATITIS; FIBROSIS PROGRESSION; CYTOKINE SIGNALING-3;

D O I：

10.3390/v1020126

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

The persistent infection with hepatitis C virus is a major cause of chronic liver disease worldwide. However, the morbidity associated with hepatitis C virus widely varies and depends on several host-related cofactors, such as age, gender, alcohol consumption, body weight, and co-infections. The objective of this review is to discuss three of these cofactors: steatosis, insulin resistance and oxidative stress. Although all may occur independently of HCV, a direct role of HCV infection in their pathogenesis has been reported. This review summarizes the current understanding and potential molecular pathways by which HCV contributes to their development.

引用

收藏

页码：126 / 143

页数：18

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