Early dystrophin disruption in the pathogenesis of experimental chronic Chagas cardiomyopathy
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2012
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Resumo
Chronic Chagas cardiomyopathy evolves over a long period of time after initial infection by Trypanosoma cruzi. Similarly, a cardiomyopathy
appears later in life in muscular dystrophies. This study tested the hypothesis that dystrophin levels are decreased in the early stage of T. cruzi infected mice that precedes the later development of a cardiomyopathy. CD1 mice were infected with T. cruzi (Brazil strain), killed at 30 and 100
days post infection (dpi), and the intensity of inflammation, percentage of interstitial fibrosis, and dystrophin levels evaluated. Echocardiography
and magnetic resonance imaging data were evaluated from 15 to 100 dpi. At 30 dpi an intense acute myocarditis with ruptured or intact
intracellular parasite nests was observed. At 100 dpi a mild chronic fibrosing myocarditis was detected without parasites in the myocardium.
Dystrophin was focally reduced or completely lost in cardiomyocytes at 30 dpi, with the reduction maintained up to 100 dpi. Concurrently,
ejection fraction was reduced and the right ventricle was dilated. These findings support the hypothesis that the initial parasitic infection-induced
myocardial dystrophin reduction/loss, maintained over time, might be essential to the late development of a cardiomyopathy in mice.
2011 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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Chronic Chagas cardiomyopathy, Dystrophin, Chagas disease, Dystrophinopathy, Trypanosoma cruzi
Citação
PRADO, Cibele M. et al. Early dystrophin disruption in the pathogenesis of experimental chronic Chagas cardiomyopathy. Microbes and Infection, Paris, v. 14, n. 1, p. 59-68, 2012. DOI: 10.1016/j.micinf.2011.08.010. Disponível em: https://linkinghub.elsevier.com/retrieve/pii/S1286-4579(11)00223-1. Acesso em: 7 fev. 2025.