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Angiotensin II and Cardiac Fibrosis

P Brecher1

  • 1Department of Biochemistry and The Cardiovascular Institute, Boston University School of Medicine,Boston, MA 02118,USA.

Trends in Cardiovascular Medicine
|January 15, 2011
PubMed

Insights

The renin-angiotensin system directly promotes cardiac fibrosis by affecting cardiac fibroblasts. Other factors, like nitric oxide, can modulate this fibrotic process.

Area of Science:

  • Cardiovascular Medicine
  • Fibrosis Research

Background:

  • The renin-angiotensin system (RAS) is implicated in cardiac fibrosis pathogenesis.
  • Both animal models and clinical studies support the RAS's role.

Purpose of the Study:

  • To review recent findings on angiotensin II's direct effects on cardiac cells.
  • To explore factors influencing angiotensin II-mediated cardiac fibrosis.

Main Methods:

  • Review of experimental animal models.
  • Analysis of clinical studies.
  • Discussion of paracrine signaling, exemplified by nitric oxide.

Main Results:

  • Angiotensin II directly acts on cardiac fibroblasts, promoting fibrosis.
  • Other factors can either enhance or reduce the fibrotic response.
  • Nitric oxide antagonizes angiotensin II's effects.

Conclusions:

  • Direct angiotensin II action on cardiac fibroblasts is a key factor in cardiac fibrosis.
  • Modulatory roles of other factors, such as nitric oxide, are significant in regulating fibrosis.

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