Calcium-binding proteins promote liver fibrosis by activating hepatic stellate cells

Chinese Academy of Sciences Institute of Biophysics Qin Zhihai research group in the new study, for the first time revealed the S100 family of calcium-binding protein S100A4 molecule by molecule activated hepatic stellate cells significantly promote liver fibrosis process.

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Icon: S100A4 gene deletion can significantly alleviate the symptoms of liver fibrosis

 

Chinese Academy of Sciences Institute of Biophysics Qin Zhihai research group in the new study, for the first time revealed the S100 family of calcium-binding protein S100A4 molecule by molecule activation process of hepatic stellate cells (HSCs) to significantly promote liver fibrosis. The outcome for the future treatment of liver fibrosis provides an important new target molecules. Related Articles published in the August 9, 2014 in the “Journal of Hepatology” magazine.

Liver fibrosis is a high incidence in the world within a range of diseases with high mortality, the liver tissue extracellular matrix (ECM) components and the abnormal deposition of hyperproliferative, pathological changes leading to structural or functional abnormalities of the liver. If the continued development of liver fibrosis, will eventually cause fatal liver failure, cirrhosis of the liver disease. China is the global incidence of cirrhosis, countries with the highest mortality rates, chronic hepatitis B patients has reached 30 million, there are more than 7 million patients with cirrhosis, liver cirrhosis five-year mortality rate of 70 to 86%, 17% -51% of liver cirrhosis will worsen liver cancer, each year about 28 million people died of cirrhosis of the liver and liver cancer.

HSCs play a very important role in the formation of the ECM, and S100A4 important molecular markers as a close relationship with fibrotic tissue fibroblasts. Qinzhi Hai study groups found in the serum and tissues of patients with liver cirrhosis S100A4 significantly increased tendency of liver fibrosis in a mouse model show that the use of macrophage-derived molecules can S100A4 gathered up by the liver tissue and α-SMA to activate HSCs cells. In vivo and in vitro experiments show that the liver S100A4 gene deletion or knockdown can significantly reduce the extent of diseased tissue fibrosis, which clearly articulate the specific molecular mechanism of S100A4 promote liver fibrosis.

In recent years, the lack of convenient treatment of chronic diseases of liver fibrosis diagnosis and effective anti-fibrotic therapy, the outcome for the future treatment of liver fibrosis provides an important new target molecules. At present, the study group of the ongoing development of a diagnostic kit based S100A4 molecule, the molecule, and liver cancer and other diseases is also an important role in the further investigation.

This work by the Chinese Academy of Sciences Institute of Biophysics Qin Zhihai research group mainly completed, get the CAS Institute of Biophysics Wang Shengdian researcher, Beijing Normal University and Peking University People’s Hospital, Professor Fan Xiaolong Professor Chen Hongsong and Beijing 302 Hospital, Professor Wang Fusheng and other great assistance. Dr. Qin Zhihai Chen Lin and Dr. Li Jie study group for co-first author of the paper, this research work has been funded by the National Science and Technology, the National Natural Science Foundation of key projects.

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