title: Hepatic fibrosis.
abstract: OBJECTIVE
  This review will summarize the most significant work that contributed to the understanding of liver fibrosis progression and resolution, which in turn has yielded new areas of therapeutic targeting.
  
  
  RESULTS
  Liver fibrosis is the result of an imbalance between production and dissolution of extracellular matrix. Stellate cells, portal myofibroblasts, and bone marrow derived cells converge in a complex interaction with hepatocytes and immune cells to provoke scarring in response to liver injury. Uncovering the specific effects of growth factors on these cells, defining the interaction of different cell population during liver fibrosis and characterizing the genetic determinants of fibrosis progression will enable the discovery of new therapeutic approaches.
  
  
  CONCLUSIONS
  The outcome of improved understanding of liver fibrosis process, especially the regulation and activation of stellate cells, is reflected in the development of new therapeutic strategies, which are validated in animal models.
authors.affiliation: Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.
authors.forename: Jingjing
authors.initials: J
authors.lastname: Jiao
authors.forename: Scott L
authors.initials: SL
authors.lastname: Friedman
authors.forename: Costica
authors.initials: C
authors.lastname: Aloman
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000818:Animals; D018450:Disease Progression; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D055166:Hepatic Stellate Cells / Q000473:pathology*; D006801:Humans; D008103:Liver Cirrhosis / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D016031:Liver Transplantation / Q000379:methods*; D011379:Prognosis
chemical_list: D020533:Angiogenesis Inhibitors; D016326:Extracellular Matrix Proteins