| First Author | Watanabe S | Year | 2007 |
| Journal | J Gastroenterol Hepatol | Volume | 22 Suppl 1 |
| Pages | S96-S100 | PubMed ID | 17567478 |
| Mgi Jnum | J:138099 | Mgi Id | MGI:3804166 |
| Doi | 10.1111/j.1440-1746.2006.04665.x | Citation | Watanabe S, et al. (2007) Non-alcoholic steatohepatitis and hepatocellular carcinoma: lessons from hepatocyte-specific phosphatase and tensin homolog (PTEN)-deficient mice. J Gastroenterol Hepatol 22 Suppl 1:S96-S100 |
| abstractText | Non-alcoholic steatohepatitis (NASH) is a term used to describe a spectrum of conditions characterized by histological findings of hepatic macrovesicular steatosis with inflammation in individuals who consume little or no alcohol. The NASH patients progress to liver cirrhosis and even hepatocellular carcinoma (HCC). Hepatocyte-specific phosphatase and tensin homolog (PTEN)-deficient mice (PTEN-deficient mice), which the authors had generated previously, showed massive hepatomegaly and steatohepatitis with triglyceride accumulation followed by liver fibrosis and HCC, a phenotype similar to human NASH. Therefore, it was shown that PTEN deficiency in hepatocytes could induce hepatic steatosis, inflammation, fibrosis and tumors and that PTEN-deficient mice were a useful animal model for not only the understanding of the pathogenesis of NASH but also the development of treatment for NASH. |
