Published online May 14, 2018. doi: 10.3748/wjg.v24.i18.1989
Peer-review started: April 4, 2018
First decision: April 27, 2018
Revised: May 1, 2018
Accepted: May 6, 2018
Article in press: May 6, 2018
Published online: May 14, 2018
Processing time: 37 Days and 7.9 Hours
As the incidence of hepatocellular carcinoma (HCC) caused by infection with the hepatotropic viruses hepatitis B and hepatitis C decreases, greater attention has become focused on HCC caused by nonalcoholic steatohepatitis (NASH), an advanced form of nonalcoholic fatty liver disease which has shown increasing prevalence in correspondence with the overall increase in metabolic syndrome over the recent decades. Several clinical population studies have shown a positive relationship between NASH and HCC, while also providing initial insights into the underlying mechanisms of HCC development from NASH. Research into the pathological progression of NASH to HCC has advanced by use of several beneficial rodent models. In this review, we summarize the established mouse models for preclinical research of NASH-associated HCC and discuss the underlying hepatic mechanisms of NASH-related tumorigenesis identified to date that could lead to new targets for treatment and prevention.
Core tip: This review provides a brief overview of the molecular mechanisms underlying progression to hepatocellular carcinoma from nonalcoholic steatohepatitis that have been identified to date using the array of mouse models currently available and popular in the experimental field.
