Role of vasoactive mediators in the pathogenesis of Chagas' disease

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article

Shankar Mukherjee¹, Huan Huang¹, Louis M. Weiss^1,2, Sylvia Costa², Julio Scharfstein³, Herbert B. Tanowitz^1,2,*

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¹ Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA

² Departments of Medicine, Albert Einstein College of Medicine, Bronx, New York

³ Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil

Academic Editor: Herbert B. Tanowitz

Front. Biosci. (Landmark Ed) 2003, 8(5), 410–419; https://doi.org/10.2741/1103

Published: 1 May 2003

(This article belongs to the Special Issue Infectious diseases of the myocardium)

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Abstract

This review focuses on the vascular pathogenesis of Chagas' disease, the cardiomyopathy caused by infection with the parasitic protozoa Trypanosoma cruzi. Recent studies strongly suggests that T. cruzi infection is linked to functional changes in the activity of two potent vasoactive peptidergic mediators, endothelin-1, a vasoconstrictor, and kinins, a group of vasodilator and pro-inflammatory peptides related to bradykinin. Understanding the molecular mechanisms underlying disturbances of vascular homoeostasis? induced by T. cruzi may provide opportunities for therapeutic intervention and amelioration of heart pathology.

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