Research Press Release | September 10, 2014
|Key Points||・Identified the cause of chronic hepatic injury of the fatty liver, and acute hepatic injury and regenerative failure due to post-operative stress.
・Clarified cellular stresses and their mechanism in fatty liver cells and identified a key molecule.
1) Clinical application in safe surgery for patients with fatty liver is expected.
2) Progress in the development of prevention methods (development of functional food products) and therapeutic methods (drug discovery) for non-alcoholic steatohepatitis (NASH) from fatty liver are expected (prevention of progression from simple fatty liver to hepatitis, liver cirrhosis and liver cancer).
|Overview||In cases where chronic and continuous liver dysfunction is observed in fatty liver, acute liver injury and impaired liver regeneration may occur immediately after surgical treatment. Some cases of chronic fatty liver have been reported to progress to NASH, liver cirrhosis, and liver cancer—issues which have been of special concern in recent years – however, the pathology of NASH is not sufficiently understood. This study successfully specified the mechanism involved in liver injury in fatty liver and regenerative failure due to surgical stress as well as identified the molecule (p62/SQSTM1) which plays a central role in this mechanism. This molecule is important in the clarification of the mechanism leading to acute injury and regenerative failure of the fatty liver, and is also involved in the progress of hepatitis (NASH), liver cirrhosis, and liver cancer. This is considered to be an important achievement from the standpoint of health science, and disease prevention, and therapy.|
Michitaka Ozaki, Professor, Graduate School of Health Sciences, Hokkaido University