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Mitochondrial reactive oxygen species as a mystery voice in hepatitis C
Author(s) -
Hino Keisuke,
Hara Yuichi,
Nishina Sohji
Publication year - 2014
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/hepr.12247
Subject(s) - steatosis , reactive oxygen species , oxidative stress , mitochondrion , insulin resistance , mitochondrial ros , hepatitis c virus , hepatocellular carcinoma , liver disease , hepatitis , hepatitis c , biology , medicine , immunology , endocrinology , cancer research , insulin , biochemistry , virus
There are several lines of evidence suggesting that oxidative stress is present in hepatitis C to a greater degree than in other inflammatory liver diseases and is closely related to disease progression. The main production site of reactive oxygen species ( ROS ) is assumed to be mitochondria, which concept is supported by evidence that hepatitis C virus ( HCV ) core protein is directly associated with them. The detoxification of ROS also is an important function of the cellular redox homeostasis system. These results draw our attention to how HCV ‐induced mitochondrial ROS production is beyond redox regulation and affects the disease progression and development of hepatocellular carcinoma ( HCC ) in chronic hepatitis C . On the other hand, HCV ‐related chronic liver diseases are characterized by metabolic alterations such as insulin resistance, hepatic steatosis and/or iron accumulation in the liver. These metabolic disorders also are relevant to the development of HCC in HCV ‐related chronic liver diseases. Here, we review the mechanisms by which HCV increases mitochondrial ROS production and offer new insights as to how mitochondrial ROS are linked to metabolic disorders such as insulin resistance, hepatic steatosis and hepatic iron accumulation that are observed in HCV ‐related chronic liver diseases.