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Mechanisms of cardiac fibrosis in inflammatory heart disease

Gabriela Kania1, Przemyslaw Blyszczuk, Urs Eriksson

  • 1Cardioimmunology, Cardiovascular Research Department, Institute of Physiology, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.

Trends in Cardiovascular Medicine
|May 8, 2010
PubMed

Insights

Monocyte-like cells in heart injury promote fibrosis and heart failure. Their progenitors drive inflammation and subsequent myocardial fibrosis, influencing heart remodeling after myocarditis.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Pathology

Background:

  • Heart injury commonly leads to pathological remodeling and fibrosis, culminating in heart failure.
  • Dilated cardiomyopathy, a major cause of heart failure, often stems from virus-induced myocarditis.
  • Monocytes and monocyte-like cells are key infiltrators at cardiac injury sites, contributing to both acute injury and chronic fibrosis.

Purpose of the Study:

  • To review the mechanisms by which heart-infiltrating monocyte-like cells contribute to cardiac remodeling and fibrosis after myocarditis.
  • To highlight the role of monocyte progenitors in the progression of heart failure.
  • To discuss the influence of cytokine balance on the fate of these progenitor cells.

Main Methods:

  • Review of recent findings on monocyte-derived cells in cardiac injury.
  • Analysis of cellular and molecular mechanisms driving fibrosis.
  • Discussion of the role of cytokines in regulating cell fate and cardiac phenotype.

Main Results:

  • Heart-infiltrating monocyte-like cells include progenitors crucial for both acute inflammation and chronic fibrosis.
  • These progenitors are a source for differentiated monocytes during inflammation and contribute to transforming growth factor-beta-mediated fibrosis.
  • A balance of pro-inflammatory and pro-fibrotic cytokines dictates cell fate and cardiac remodeling.

Conclusions:

  • Bone marrow-derived progenitors within heart-infiltrating monocytes play a critical role in myocarditis-induced heart failure.
  • Understanding these mechanisms is vital for targeting pathological remodeling and fibrosis.
  • Cytokine milieu critically influences the progression from inflammation to fibrosis and heart failure.

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