Portal hypertension and vascular biology of the liver
Portal hypertension is the most serious complication of liver cirrhosis. Our goal is to understand the mechanisms of portal hypertension in liver cirrhosis and develop therapies that ameliorate detrimental consequences, such as varices and ascites, associated with portal hypertension. We are also interested in how the lymphatic vascular system in general and lymphangiogenesis in particular are mechanistically related to the pathogenesis and maintenance of liver diseases.
Currently there is no effective treatment for liver fibrosis. Furthermore, liver cirrhosis, an advanced stage of fibrosis, is the major cause of portal hypertension. Our recent studies showed Nogo-B, a.k.a., reticulon 4B, promotes liver fibrosis/cirrhosis and the development of portal hypertension.
Nitric oxide signaling in endothelial cells
Nitric oxide (NO) is one of the most important vasodilator molecules. Besides its traditional role as a vasodilator, NO has recently received attention as a regulator of endothelial cell functions. We have published a very fundamental study in this area that suggests the Golgi apparatus is a favorable site of S-nitrosylation.