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Gene Expression Changes Associated with Myocarditis and Fibrosis in Hearts of Mice with Chronic Chagasic Cardiomyopathy
Author(s) -
Milena Botelho Pereira Soares,
Ricardo Santana de Lima,
Leonardo Lima Rocha,
Juliana Fraga Vasconcelos,
Sílvia Regina Rogatto,
Ricardo Ribeiro dos Santos,
Sanda Iacobaş,
Regina Coeli dos Santos Goldenberg,
Dumitru A. Iacobaş,
Herbert B. Tanowitz,
Antônio Carlos Campos de Carvalho,
David C. Spray
Publication year - 2010
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/653481
Subject(s) - trypanosoma cruzi , fibrosis , pathogenesis , chagas disease , myocarditis , immunology , cardiomyopathy , extracellular matrix , heart failure , biology , immune system , inflammation , medicine , pathology , genetics , parasite hosting , world wide web , computer science
Chronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis in the heart. We performed an extensive microarray analysis of hearts from a mouse model of this disease and identified significant alterations in expression of approximately 12% of the sampled genes. Extensive up-regulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins, and major histocompatibility complex molecules) and fibrosis (extracellular matrix components, lysyl oxidase, and tissue inhibitor of metalloproteinase 1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide new therapeutic targets in chronic Chagas disease.

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