The identification and isolation of hepatic stellate cells (HSCs) as the main fibrogenic cells in liver, as well as techniques to establish cultured HSC lines have enabled significant progress in understanding key events in the transdifferentiation process of quiescent HSCs to fibrogenic myofibroblasts. Hepatic fibrosis due to chronic liver disease represents a major global health burden. Cirrhosis is characterized by fibrous septae that are present throughout the liver, subdividing the organ into parenchymal nodules, which may vary between micronodules or macronodules. HSC-specific genetic deletion of autophagy related protein 7 in murine models of liver fibrosis and in cultured HSCs both lead to reduced fibrogenesis. Liver injury leads to activation of HSCs and subendothelial extracellular matrix deposition, promoting capillarization of liver sinusoids that increases resistance to blood flow and compromises oxygen delivery. Adipokine signaling has emerged as an important regulator of HSC activation in the context of metabolic syndrome.

Original languageEnglish
Title of host publicationThe Liver
Subtitle of host publicationBiology and Pathobiology
Number of pages11
ISBN (Electronic)9781119436812
ISBN (Print)9781119436829
StatePublished - 24 Jan 2020


  • Cirrhosis
  • Fibrogenesis
  • Hepatic fibrosis
  • Hepatic stellate cells
  • Liver injury
  • Metabolic syndrome


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