Liver cholestatic diseases, which stem from diverse etiologies, result in liver toxicity and fibrosis and may progress to cirrhosis and liver failure. We show that CCN1 (also known as CYR61), a matricellular protein that dampens and resolves liver fibrosis, also mediates cholangiocyte proliferation and ductular reaction, which are repair responses to cholestatic injury. In cholangiocytes, CCN1 activated NF-κB through integrin αvβ5/αvβ3, leading to
Ki-Hyun Kim, Chih-Chiun Chen, Gianfranco Alpini, Lester F. Lau
CCN1 is highly elevated in cholangiocytes in human and murine cholestatic livers.