Liver fibrosis is the outcome of several chronic liver injuries such as viral, metabolic or autoimmune diseases. In humans this process leads to fibrotic scarring of liver tissue and end stage liver cirrhosis. Hepatic fibrosis is characterized by differentiation of quiescent hepatic stellate cells into activated myofibroblasts. Whereas quiescent hepatic stellate cells are the involved in vitamin A storage in the liver, activated myofibroblasts are the major source for extracellular matrix production and accumulation of collagen type I. Hepatic scarring and collagen deposition is closely regulated by pro- and anti-inflammatory cytokines. The TGF-b signaling network is one of the central regulators mediating liver fibrosis. Furthermore its ligands and receptors play important roles in angiogenesis and cancer development.

Our work focuses on stellate cell pathology in response to liver injury. We therefore investigate cytokine signaling with special focus on proteins involved in TGF-b signal transduction. One of these receptors/ligands is Endoglin (CD105). Endoglin is a type III auxiliary TGF-b receptor that modulates pro- and antifibrotic effects of TGF-b signal transduction. It also plays important roles in angioneogenesis and cancer development. Our research group analyzes the effect of Endoglin on TGF-b signaling in these conditions, characterizing modulatory effects of Endoglin deficiency or overexpression.