Abstract

Sustained progress in defining the molecular pathophysiology of hepatic fibrosis has led to a comprehensive framework for developing antifibrotic therapies. Indeed, the single greatest limitation in bringing new drugs to the clinical setting is a lack of clarity regarding clinical trial and treatment end points, not a lack of promising agents. A range of treatments, including those developed for other indications, as well as those specifically developed for hepatic fibrosis, are nearing or in clinical trials. Most are focused on attacking features of either hepatic injury and/or activated stellate cells and myofibroblasts, which are the primary sources of extracellular matrix (scar) proteins. Thus, features of injury and stellate cell activation provide a useful template for classifying these emerging agents and point to a new class of therapies for patients with fibrosing liver disease.

Original languageEnglish
Pages (from-to)803-816
Number of pages14
JournalExpert Review of Gastroenterology and Hepatology
Volume2
Issue number6
DOIs
StatePublished - 2008

Keywords

  • Cirrhosis
  • Cytokine
  • Cytokine receptor
  • Hepatic fibrosis
  • Hepatoprotection
  • Liver fibrosis
  • Matrix degradation
  • Myofibroblast
  • Stellate cell

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