Abstract

Multiple etiologies of liver disease lead to liver fibrosis through integrated signaling networks that regulate the deposition of extracellular matrix. This cascade of responses drives the activation of hepatic stellate cells (HSCs) into a myofibroblast-like phenotype that is contractile, proliferative and fibrogenic. Collagen and other extracellular matrix (ECM) components are deposited as the liver generates a wound-healing response to encapsulate injury. Sustained fibrogenesis leads to cirrhosis, characterized by a distortion of the liver parenchyma and vascular architecture. Uncovering the intricate mechanisms that underlie liver fibrogenesis forms the basis for efforts to develop targeted therapies to reverse the fibrotic response and improve the outcomes of patients with chronic liver disease.

Original languageEnglish
Pages (from-to)195-206
Number of pages12
JournalBest Practice and Research: Clinical Gastroenterology
Volume25
Issue number2
DOIs
StatePublished - Apr 2011

Keywords

  • Adipokines
  • Fibrogenesis
  • Growth factors
  • Immune cells
  • Stellate cell
  • Tyrosine kinase

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