Hepatic fibrosis and the renin-angiotensin system

Am J Ther. 2011 Nov;18(6):e202-8. doi: 10.1097/MJT.0b013e3181df8df5.

Abstract

The renin-angiotensin system (RAS) is involved in hepatic fibrosis. To date there is no known effective treatment for hepatic fibrosis. Modulation of the RAS with angiotensin converting enzyme inhibitors and angiotensin receptor blockers may be a promising therapeutic option for the treatment of hepatic fibrosis. This review provides an update about the role of RAS in hepatic fibrosis, and treatment of hepatic fibrosis in the light of different studies in animals and humans is also updated. RAS induces key steps involved in hepatic fibrosis, such as activation of hepatic stellate cells and expression of transforming growth factor β1. Treatment with angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers attenuate fibrosis progression in both animal and human studies. Further, controlled studies are required to evaluate the role of RAS inhibitors and angiotensin-converting enzyme 2 in patients with chronic liver diseases in whom the causative agent cannot be removed.

Publication types

  • Review

MeSH terms

  • Angiotensin Receptor Antagonists / therapeutic use*
  • Angiotensin-Converting Enzyme 2
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Animals
  • Hepatic Stellate Cells / drug effects
  • Hepatic Stellate Cells / physiology
  • Humans
  • Liver Cirrhosis / drug therapy*
  • Liver Cirrhosis / physiopathology*
  • Peptidyl-Dipeptidase A / physiology
  • Renin-Angiotensin System / drug effects
  • Renin-Angiotensin System / physiology*
  • Transforming Growth Factor beta1 / drug effects
  • Transforming Growth Factor beta1 / physiology

Substances

  • Angiotensin Receptor Antagonists
  • Angiotensin-Converting Enzyme Inhibitors
  • Transforming Growth Factor beta1
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2