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Fibrosis, a common pathway to organ failure: angiotensin II and tissue repair

K T Weber1

  • 1Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia, USA.

Seminars in Nephrology
|October 8, 1997
PubMed

Insights

Fibrosis, a common pathway to organ failure, involves angiotensin II (ANG II) and TGF-beta 1. Blocking these pathways with ACE inhibitors or AT1 receptor antagonists can prevent fibrosis and protect organs.

Area of Science:

  • Cardiovascular Science
  • Nephrology
  • Pulmonology
  • Hepatology
  • Pathophysiology

Background:

  • Fibrosis is a common mechanism leading to heart, kidney, lung, and liver failure.
  • Understanding fibrosis pathophysiology is crucial for developing protective pharmacological strategies.
  • Tissue repair involves inflammatory cells and myofibroblasts, which are key in collagen turnover.

Purpose of the Study:

  • To elucidate the pathophysiologic mechanisms underlying organ fibrosis.
  • To investigate the role of angiotensin II (ANG II) in fibrosis development.
  • To explore the potential of targeting the renin-angiotensin system for antifibrotic therapies.

Main Methods:

  • Review of cellular and molecular events in tissue repair and fibrosis.
  • Analysis of the autocrine/paracrine signaling of ANG II.
  • Examination of the role of transforming growth factor-beta 1 (TGF-beta 1) in fibroblast activation.

Main Results:

  • De novo generation of ANG II occurs during tissue repair.
  • ANG II regulates TGF-beta 1 expression via AT1 receptor binding.
  • TGF-beta 1 mediates fibroblast to myofibroblast differentiation and collagen production.

Conclusions:

  • Angiotensin-converting enzyme (ACE) inhibition and AT1 receptor antagonism mitigate fibrosis.
  • Targeting the renin-angiotensin system offers protective interventions against organ fibrosis.
  • Understanding these mechanisms provides a basis for novel antifibrotic drug development.

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