{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T17:39:36Z","timestamp":1790271576720,"version":"4.1.0"},"reference-count":77,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,1,8]],"date-time":"2014-01-08T00:00:00Z","timestamp":1389139200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hepatology Research"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:p>There are several lines of evidence suggesting that oxidative stress is present in hepatitis <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content> 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 (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) is assumed to be mitochondria, which concept is supported by evidence that hepatitis <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content> virus (<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>) core protein is directly associated with them. The detoxification of <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> also is an important function of the cellular redox homeostasis system. These results draw our attention to how <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010induced mitochondrial <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> production is beyond redox regulation and affects the disease progression and development of hepatocellular carcinoma (<jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content>) in chronic hepatitis <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>. On the other hand, <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010related 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 <jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010related chronic liver diseases. Here, we review the mechanisms by which <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> increases mitochondrial <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> production and offer new insights as to how mitochondrial <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> are linked to metabolic disorders such as insulin resistance, hepatic steatosis and hepatic iron accumulation that are observed in <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010related chronic liver diseases.<\/jats:p>","DOI":"10.1111\/hepr.12247","type":"journal-article","created":{"date-parts":[[2013,10,12]],"date-time":"2013-10-12T01:04:07Z","timestamp":1381539847000},"page":"123-132","source":"Crossref","is-referenced-by-count":23,"title":["Mitochondrial reactive oxygen species as a mystery voice in hepatitis 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