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Xinhua News Agency, Tokyo, July 28 (Reporter Qian Zheng) Yokohama City University in Japan recently issued a press release saying that the research team involved in the university used human iPS cells (human induced pluripotent stem cells) to cultivate liver organoids. Transplanting these artificial liver organoids into experimental mice with liver fibrosis can improve the symptoms of liver fibrosis. This research will help develop new treatments for liver cirrhosis.

The communiqué said that cirrhosis is a fatal chronic liver disease that can be caused by viral infection, fatty liver and alcoholic liver damage. There is no cure except for liver transplantation, which faces a serious shortage of donors. In the early stages of cirrhosis, liver fibrosis usually occurs. If it continues to develop, liver function will decline significantly. Therefore, controlling the process of liver fibrosis is very important to prevent cirrhosis.

Since the fetal liver has a strong tissue reconstruction ability during development, researchers came up with the idea of ​​using human iPS cells to cultivate fetal liver organoids as a regenerative medicine method. In this study, researchers from Yokohama City University and the University of Tokyo constructed a mouse model of liver fibrosis and transplanted the liver of a mid-pregnancy mouse fetus onto its liver surface. They found that the survival rate of mice with liver fibrosis was significantly improved and the symptoms of liver fibrosis were also improved.

Next, the researchers used human iPS cells to cultivate artificial liver organoids that were similar to the fetal liver of mid-pregnancy mice, with structures such as hepatic sinusoids and bile ducts. After transplanting these artificial liver organoids into mice with liver fibrosis, their survival rate and symptoms of liver fibrosis were improved, and various liver function indicators also improved. The study also showed that after transplanting artificial liver organoids, immature macrophages in mice with liver fibrosis were induced to differentiate into anti-inflammatory macrophages, thereby partially reversing liver fibrosis.

The relevant paper has been published in the American journal Science Translational Medicine. (End)