The most "true" slow plus acute liver failure mouse model was successfully constructed

The team of Professors Xiang Xiaogang and Xie Qing of Ruijin Hospital, affiliated with Shanghai Jiaoxuan University School of Medicine, worked with Professor Gao Bin of the National Institute of Alcohol Abuse and Alcoholism to build for the first time a mouse model that is closest to the clinical characteristics of chronic and acute liver failure, and solved the dilemma of mechanism research and new drug development in the field of chronic and acute liver failure, which has been lacking in effective mouse disease models. The findings were published recently in the Journal of Healing.
and acute liver failure (ACLF) is a type of severe clinical syndrome characterized by acute liver function loss, liver organ damage and short-term high mortality on the basis of chronic liver disease. China's chronic liver disease population base is large, of which slow and acute liver failure is the main type of liver failure in China. Clinical data show that the incidence of chronic and acute liver failure in hospitalized liver cirrhosis population is 24% to 40%, and its condition is dangerous, complications are many, lack of liver regenerative drugs, treatment difficulties, mortality rate is very high, seriously affecting the life and health of our people and socio-economic development.
, however, there is currently no breakthrough in the clinical treatment of chronic and acute liver failure. In basic studies, the lack of ideal small animal models of chronic and acute liver failure greatly limits the study of pathogenesis and the screening of follow-up clinical intervention targets.
In this study, the researchers pioneered the "three-stage molding method" of chronic and acute liver failure, and for the first time in the world established a mouse model of slow plus acute liver failure that is closest to the clinical characteristics of patients, successfully achieving a complete simulation of the core pathogenesis of most patients with chronic and acute liver failure in mouse models, and the model can also be a good simulation of liver external organ damage, such as kidney damage and multi-organ failure, with a suitable survival cycle for intervention studies. At the same time, the model molding method can be well standardized, easy to obtain materials, simple and fast, easy to popularize, for slow and acute liver failure related mechanism research and new treatment target screening provides a reliable platform.
At the same time, the research team found that the hepatic STAT1/STAT3 activation imbalance affects liver regeneration as an important mechanism for the progression of the course of chronic and acute liver failure, and this mouse model confirmed for the first time that by interfering with the intra-liver STAT1/STAT3 activation imbalance, the prognosis of mice with chronic and acute liver failure was improved, and found that the new cytokine leukokin 22 (IL-22) can regulate the hepatic STAT1/STAT3 activation imbalance. The research results provide a new strategy of immunotherapy for patients' clinical treatment, and promoting the clinical research of this program will bring more hope for the rehabilitation of the large population of chronic liver patients in China.
Frank Tacke, deputy editor-in-chief of Journal of Hepatology, written in the same journal
Huang Xin Tang Wenjia