Liver fibrosis, and its outcome, cirrhosis, result from an imbalance in extracellular matrix synthesis and degradation. This process is mediated mainly by activated hepatic stellate cells (HSC) undergoing a phenotypic switch from a quiescent vitamin A storing phenotype to a proliferative myofibroblast-like cell. Cirrhosis represents a serious worldwide health care problem and may be caused by genetic disorders, viruses, toxins, auto-immune, and cholestatic diseases. Liver transplantation is a highly successful treatment for end-stage cirrhosis, with a 5-year survival rate of around 70percent. However, limited availability of organs and comorbid factors are still major problems.
Animal models of chronic liver injury showed that transplantation of bone marrow cells (BMC) can improve liver function, as well as the survival rate, although through mechanisms not fully understood. Both cell fusion and transdifferentiation into hepatocytes have been reported. Although these events seem to be very rare (less than 0.5%), suggesting that other mechanisms are involved in liver regeneration mediated by BMC. However, data on this issue were obtained in animal models of liver disease induced by toxins (as CCl4 or acetaminophen), whose mechanisms differ from those of cholestatic liver diseases, one of the main causes of liver failure in children.
Last date updated on July, 2014