日野 啓輔
   Department     ,
   Position  
Article types 総説
Language English
Peer review Peer reviewed
Presence of invitation Invited paper
Title Mitochondrial damage and iron metabolic dysregulation in hepatitis C virus infection
Journal Formal name:Free Radical Biology and Medicine
Abbreviation:Free Radic Biol Med
Domestic / ForeginForegin
Volume, Issue, Page 133,193-199頁
Author and coauthor Hino K, Nishina S, Sasaki K, Hara Y
Publication date 2019
Summary Hepatitis C virus (HCV) infection often leads to chronic hepatitis that can progress to liver cirrhosis and hepatocellular carcinoma (HCC). Although HCV infection is expected to decrease due to the high rate of HCV eradication via the rapid dissemination and use of directly acting antivirals, HCV infection remains a leading cause of HCC. Although the mechanisms underlying the HCC development are not fully understood, oxidative stress is present to a greater degree in HCV infection than in other inflammatory liver diseases and has been proposed as a major mechanism of liver injury in patients with chronic hepatitis C. Hepatocellular mitochondrial alterations and iron accumulation are well-known characteristics in patients with chronic hepatitis C and are closely related to oxidative stress, since the mitochondria are the main site of reactive oxygen species generation, and iron produces hydroxy radicals via the Fenton reaction. In addition, phlebotomy is an iron reduction approach that aims to lower serum transaminase levels in patients with chronic hepatitis C. Here, we review and discuss the mechanisms by which HCV induces mitochondrial damage and iron accumulation in the liver and offer new insights concerning how mitochondrial damage and iron accumulation are linked to the development of HCC.