Dysregulation of coagulation and fibrinolytic factors is now being recognized as not just a late-stage sequelae of liver disease, but in fact one of the potential contributing risk factors for liver cirrhosis. Recent molecular and animal studies have uncovered intriguing roles for plasmin and the plasminogen activators in protecting the liver from fibrosis development in a manner that is largely fibrin-independent. These pleiotropic effects may be explained by functions of their other proteolytic targets (e.g. hepatocyte growth factor) and receptor-mediated signaling. This review features salient basic science research which shows the immense potential of promoting the hepatic activity of plasmin and its activators in the prevention and treatment of liver cirrhosis in humans.
Keywords: Fibrinolysis, hepatic stellate cell, hepatocyte growth factor, liver fibrosis, plasminogen, plasminogen activator inhibitor-1, tissue-type plasminogen activator, urokinase plasminogen activator, fibrinolytic factors, hepatocyte growth factor), coagulation cascade, Pro-fibrotic cytokines, extracellular matrix components, coagulation factors, carbon tetrachloride
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