Researchers from the Second Military Medical University and Inner Mongolia University found that aging liver cells obtained from aging mice after continuous transplantation regained their youth and fully restored their proliferation ability. The researchers achieved the same results on human liver cells. The results show that the "polyploid mediators" of liver cells are regulated differently during aging and regeneration.
The liver is the main organ of human metabolism. As we all know, it participates in the metabolism of various substances in the body, such as synthesis, decomposition and excretion. When liver dysfunction occurs, the entire body is affected. Alcoholic cirrhosis, viral hepatitis, liver cirrhosis, hepatocellular carcinoma, cholestatic cirrhosis and many other liver diseases are common in the elderly. With age, the structure or function of the liver will also undergo some changes, which decreases Improved resistance to various diseases, aggravated primitive liver disease, and made a healthy liver more susceptible to various diseases.
A detailed understanding of the aging mechanism of liver cells may help treat age-related liver disease processes. In this article, the researchers confirmed that ploidy hepatocytes of old mice accumulate in the liver of old mice. It is related to the accumulation of DNA damage and the activation of p53-p21 and p16ink4a-pRB signaling pathways. It is difficult to induce multiple continuous cell divisions in any animal model. Here, the researchers placed mice lacking Fah-/-acetylhydrolase (Fah-/-) under continuous liver cell transplantation. They studied the senescence of liver cells, which have undergone long-term cell proliferation for 12 consecutive transplants. Researchers have discovered that the proliferation of liver cells can prevent aging and always stay young. Telomerase activation in liver cells after continuous transplantation is related to the reversal of aging.
In the case of continuous transplantation, the senescent hepatocytes obtained from aging mice completely restored their youth and proliferation ability. The researchers also obtained the same results on human liver cells. After continuous transplantation, octoploid hepatocytes dropped from the initial high rate to a low level comparable to that of young liver. These results indicate that the "polyploid cones" of hepatocytes are regulated differently during aging and regeneration. Related research findings on reversing liver cell senescence may promote future research on liver senescence and cell therapy.