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World J Gastroenterol. Sep 21, 2014; 20(35): 12381-12390
Published online Sep 21, 2014. doi: 10.3748/wjg.v20.i35.12381
Smad3 phospho-isoform signaling in hepatitis C virus-related chronic liver diseases
Takashi Yamaguchi, Katsunori Yoshida, Miki Murata, Koichi Matsuzaki
Takashi Yamaguchi, Katsunori Yoshida, Miki Murata, Koichi Matsuzaki, Department of Gastroenterology and Hepatology, Kansai Medical University, Osaka 570-8506, Japan
Author contributions: Yamaguchi T, Yoshida K, Murata M and Matsuzaki K performed the research and analyzed the data; Yamaguchi T and Matsuzaki K wrote the paper.
Correspondence to: Takashi Yamaguchi, MD, PhD, Department of Gastroenterology and Hepatology, Kansai Medical University, 10-15 Fumizonocho, Moriguchi, Osaka 570-8506, Japan. yamaguct@takii.kmu.ac.jp
Telephone: +81-6-69961001 Fax: +81-6-69964874
Received: November 27, 2013
Revised: February 22, 2014
Accepted: May 29, 2014
Published online: September 21, 2014
Processing time: 296 Days and 3.9 Hours
Core Tip

Core tip: The risk of hepatocellular carcinoma (HCC) development increases in patients persistently infected with hepatitis viruses, especially in patients with active viral replication and inflammation. Our model suggests that the chronic inflammatory state and the hepatitis viruses themselves act in concert with genetic or epigenetic alterations to worsen human liver diseases by promoting hepatic carcinogenesis. The affected hepatocytes are subject to such interactions until their descendants acquire other genetic or epigenetic alterations. Even after the withdrawal of promoters such as chronic inflammation and hepatitis viruses, the hepatocytes could retain proliferative phenotypes, enabling some pre-neoplastic hepatocytes to develop into HCC.