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.
|Original language||English (US)|
|Journal||Frontiers in bioscience : a journal and virtual library|
|State||Published - May 1 2003|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Immunology and Microbiology(all)