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Dysregulation of Liver Regeneration by Hepatitis B Virus Infection: Impact on Development of Hepatocellular Carcinoma.
Park, Eun-Sook; Dezhbord, Mehrangiz; Lee, Ah Ram; Park, Bo Bae; Kim, Kyun-Hwan.
Afiliación
  • Park ES; Institute of Biomedical Science and Technology, School of Medicine, Konkuk University, Seoul 05029, Korea.
  • Dezhbord M; Department of Precision Medicine, School of Medicine, Sungkyunkwan University, Suwon 16419, Korea.
  • Lee AR; Department of Precision Medicine, School of Medicine, Sungkyunkwan University, Suwon 16419, Korea.
  • Park BB; Institute of Biomedical Science and Technology, School of Medicine, Konkuk University, Seoul 05029, Korea.
  • Kim KH; Department of Precision Medicine, School of Medicine, Sungkyunkwan University, Suwon 16419, Korea.
Cancers (Basel) ; 14(15)2022 07 22.
Article en En | MEDLINE | ID: mdl-35892823
ABSTRACT
The liver is unique in its ability to regenerate in response to damage. The complex process of liver regeneration consists of multiple interactive pathways. About 2 billion people worldwide have been infected with hepatitis B virus (HBV), and HBV causes 686,000 deaths each year due to its complications. Long-term infection with HBV, which causes chronic inflammation, leads to serious liver-related diseases, including cirrhosis and hepatocellular carcinoma. HBV infection has been reported to interfere with the critical mechanisms required for liver regeneration. In this review, the studies on liver tissue characteristics and liver regeneration mechanisms are summarized. Moreover, the inhibitory mechanisms of HBV infection in liver regeneration are investigated. Finally, the association between interrupted liver regeneration and hepatocarcinogenesis, which are both triggered by HBV infection, is outlined. Understanding the fundamental and complex liver regeneration process is expected to provide significant therapeutic advantages for HBV-associated hepatocellular carcinoma.
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Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: Cancers (Basel) Año: 2022 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: Cancers (Basel) Año: 2022 Tipo del documento: Article