Fig. 1.

Mechanisms of parenchymal repair in the adult liver after injury. Schematic micrograph showing the contribution made by hepatocytes vs. hepatic progenitor cells (HPCs) to parenchymal repair under conditions of biliary or hepatocyte damage. In response to biliary injury there is mobilisation and proliferation of hepatic progenitor cells within a laminin rich niche via myofibroblast-derived signals including Jagged1 to activate the ‘ductular reaction’. In contrast, hepatocyte targeted injuries including partial hepatectomy stimulate hepatocytes to enter mitosis and restore liver mass. In the absence of additional superimposed injury, this capacity is almost infinite (up to 90% of liver volume can be resected in rat), but becomes overwhelmed following chronic or fulminant damage when hepatocytes either undergo necrosis or become increasingly senescent. It is thought phagocytosis of hepatocyte debris stimulates the HPC response via signals including macrophage-derived Wnt. PV portal vein, HA hepatic artery, MF myofibroblast, ECM extracellular matrix