What's new in liver fibrosis? The origin of myofibroblasts in liver fibrosis

J Gastroenterol Hepatol. 2012 Mar;27 Suppl 2(Suppl 2):65-8. doi: 10.1111/j.1440-1746.2011.07002.x.


Chronic liver injury of many etiologies produces liver fibrosis and may eventually lead to the formation of cirrhosis. Fibrosis is part of a dynamic process associated with the continuous deposition and resorption of extracellular matrix, mainly fibrillar collagen. Studies of fibrogenesis conducted in many organs including the liver demonstrate that the primary source of the extracellular matrix in fibrosis is the myofibroblast. Hepatic myofibroblasts are not present in the normal liver but transdifferentiate from heterogeneous cell populations in response to a variety of fibrogenic stimuli. Debate still exists regarding the origin of hepatic myofibroblasts. It is considered that hepatic stellate cells and portal fibroblasts have fibrogenic potential and are the major origin of hepatic myofibroblasts. Depending on the primary site of injury the fibrosis may be present in the hepatic parenchyma as seen in chronic hepatitis or may be restricted to the portal areas as in most biliary diseases. It is suggested that hepatic injury of different etiology triggers the transdifferentiation to myofibroblasts from distinct cell populations. Here we discuss the origin and fate of myofibroblast in liver fibrosis.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cell Differentiation*
  • Cell Lineage*
  • Epithelial-Mesenchymal Transition
  • Extracellular Matrix / metabolism
  • Extracellular Matrix / pathology
  • Fibrillar Collagens / metabolism
  • Humans
  • Liver / metabolism
  • Liver / pathology*
  • Liver Cirrhosis / etiology
  • Liver Cirrhosis / metabolism
  • Liver Cirrhosis / pathology*
  • Myofibroblasts / metabolism
  • Myofibroblasts / pathology*


  • Fibrillar Collagens