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Role of endothelin 1 in the pathogenesis of chronic chagasic heart disease

Herbert B Tanowitz1, Huan Huang, Linda A Jelicks

  • 1Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461, USA. tanowitz@aecom.yu.edu

Infection and Immunity
|March 24, 2005
PubMed

Insights

Endothelin 1 (ET-1) contributes to Chagasic cardiomyopathy. Deleting the ET-1 gene in cardiac myocytes reduced fibrosis and protected against heart dysfunction following Trypanosoma cruzi infection.

Area of Science:

  • Cardiovascular Research
  • Infectious Diseases
  • Molecular Biology

Background:

  • Endothelin 1 (ET-1) is implicated in the pathogenesis of Chagasic cardiomyopathy.
  • Previous studies suggest a role for ET-1 in the cardiac complications of Chagas disease.

Purpose of the Study:

  • To investigate the specific role of ET-1 in cardiac myocytes and endothelial cells in the development of Chagasic cardiomyopathy.
  • To determine if targeted deletion of ET-1 affects the progression of Trypanosoma cruzi-induced heart disease.

Main Methods:

  • Utilized cell-specific ET-1 knockout mouse models (ET-1flox/flox;alpha-MHC-Cre(+) and ET-1flox/flox;Tie 2 Cre(+)) infected with Trypanosoma cruzi.
  • Assessed cardiac pathology, including inflammation and fibrosis, 130 days post-infection.
  • Employed cardiac magnetic resonance imaging and echocardiography to evaluate cardiac function and structure.

Main Results:

  • All infected mice survived the acute phase; inflammation and fibrosis were present in all groups.
  • Fibrosis was significantly reduced in ET-1flox/flox;alpha-MHC-Cre(+) mice (cardiac myocyte-specific deletion).
  • Cardiac magnetic resonance imaging showed no increase in right ventricular internal diameter in ET-1flox/flox;alpha-MHC-Cre(+) mice, unlike other infected groups.
  • Echocardiography revealed attenuated left ventricular dysfunction in ET-1flox/flox;alpha-MHC-Cre(+) mice compared to controls.

Conclusions:

  • Cardiac myocyte-derived ET-1 plays a crucial role in the pathogenesis of chronic Chagasic cardiomyopathy.
  • Targeting ET-1 in cardiac myocytes may offer a therapeutic strategy for Chagas disease-related heart conditions.

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