Activation of lymphangiogenesis by platelet as novel therapeutic approaches for liver cirrhosis and portal hypertension.

This letter comments on the recently published article in the , in which the authors demonstrated a strong link between lymphangiogenesis and the process of platelet adherence, aggregation, and activation by employing a rat model of liver cirrhosis caused by bile duct ligation (BDL). The authors applied both gain and loss of function approach by using platelet-rich plasma and vascular endothelial growth factor 3 receptor inhibitor MAZ-51 to activate and inhibit angiogenetic signaling in BDL rat model, respectively, to verify the crucial function of lymphangiogenesis in the development of liver cirrhosis and portal hypertension (PHT). In clinical practice, platelet transfusion has been applied to improve liver function in patients suffering from chronic liver disease and cirrhosis. Therefore, this study provides support for the application of platelet transfusion or pharmacological intervention of lymphangiogenesis as novel therapeutic approaches for liver cirrhosis and PHT.