Nonalcoholic steatohepatitis (NASH), the most severe form of nonalcoholic fatty liver disease (NAFLD), can increase the risk of liver failure and liver cancer. No drug is available to slow or stop NASH. A new research appearing in the journal Cell Metabolism now provides a way to reverse liver damage associated with NASH. The study, carried out by Dr Xiaobo Wang and other researchers from Columbia University Medical Center (CUMC), shows that targeting the TAZ protein can stop and even reverse fibrosis in the liver of mice. Nonalcoholic fatty liver disease (NAFLD) is a group of diseases affecting people who drink little to no alcohol. It is characterized by the buildup of extra fat in liver cells. According to estimates, 20% of people in the USA suffer from NAFLD, and the number is growing because of the increasing prevalence of obesity. A significant percentage of this population will develop NASH, which is associated with higher risk of liver failure and liver cancer. Some scientists believe that inflammation is the driving force underlying NASH and the progression to fibrosis. It has been reported that high levels of liver fibrosis increases the risk of death from NASH. But the molecular basis of NASH is still unclear, which has limited the development of drugs. In this study, Dr Xiaobo Wang and colleagues set out to find methods to halt liver fibrosis in NASH mice. They discovered that a protein called TAZ actually has a role in initiating fibrosis: TAZ is much higher in liver cells of human and mouse NASH liver than in normal or steatotic liver. When the researchers silenced TAZ in liver cells of a NASH mouse model, fibrosis in the liver was stopped and existing fibers were dissolved. Moreover, the inactivation of TAZ decreased liver inflammation and cell death. CusAb offers Recombinant HTR2C and HRP conjugated antibody. Dr Wang and colleagues also analyzed liver biopsy specimens from patients with NAFLD or NASH, and they assumed that TAZ works the same in humans. Further investigation showed that TAZ could be a factor that contributes to the progression of NASH.
