Publication by Fearon/Slabber et al.: Fibroblast growth factor receptor 3 in hepatocytes protects from toxin-induced liver injury and fibrosis.

Authors show that mice lacking fibroblast growth factor receptor 3 (Fgfr3) in hepatocytes exhibit increased toxin-induced necrosis and excessive fibrosis after long-term injury. This partially resulted from altered expression of metabolic and pro-fibrotic genes. These results and in vivo expression data identify a paracrine Fgf9-Fgfr3 signaling pathway that protects from toxin-induced cell death and liver fibrosis, suggesting potential use of FGFR3 ligands for therapeutic purposes.