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IMPLICATION OF TRANSFORMING GROWTH FACTOR-BETA1 IN CHAGAS DISEASE MYOCARDIOPATHY
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Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Departamento de Ultra-Estrutura e Biologia Celular. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Departamento de Ultra-Estrutura e Biologia Celular. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Departamento de Pesquisa Clínica. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Departamento de Pesquisa Clínica. Rio de Janeiro, RJ, Brasil.
University of São Paulo. Heart Institute. Service of Pathology. São Paulo, SP, Brazil.
INSERM 105. Commissariat à l’Energie Atomique. Department of Cellular Responses and Dynamics. Grenoble, France.
INSERM 105. Commissariat à l’Energie Atomique. Department of Cellular Responses and Dynamics. Grenoble, France.
INSERM 105. Commissariat à l’Energie Atomique. Department of Cellular Responses and Dynamics. Grenoble, France.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Departamento de Ultra-Estrutura e Biologia Celular. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Departamento de Pesquisa Clínica. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Departamento de Pesquisa Clínica. Rio de Janeiro, RJ, Brasil.
University of São Paulo. Heart Institute. Service of Pathology. São Paulo, SP, Brazil.
INSERM 105. Commissariat à l’Energie Atomique. Department of Cellular Responses and Dynamics. Grenoble, France.
INSERM 105. Commissariat à l’Energie Atomique. Department of Cellular Responses and Dynamics. Grenoble, France.
INSERM 105. Commissariat à l’Energie Atomique. Department of Cellular Responses and Dynamics. Grenoble, France.
Abstract
Cardiac dysfunction with progressive fibrosis is a hallmark of Chagas disease. To evaluate the involvement of transforming growth factor (TGF)-beta1 in this disease, TGF-beta1 levels in patients were measured at 3 stages: asymptomatic indeterminate (IND), cardiac with no or slight heart dysfunction (Card 1), and cardiac with moderate or severe heart dysfunction (Card 2). All patients had significantly higher circulating levels of TGF-beta1 than did healthy persons, and 27% of patients in the Card 1 group had higher TGF-beta1 levels than did patients in the IND group. Immunohistochemical analysis of cardiac biopsy specimens showed strong fibronectin staining in the extracellular matrix and staining for phosphorylated Smad 2 (activation of the TGF-beta1 signaling pathway) in cell nuclei. The higher levels of latent TGF-beta1 observed in patients with myocardiopathy, together with intracellular activation of the TGF-beta1 pathway and tissue fibrosis, suggest that TGF-beta1 plays an important role in Chagas disease. TGF-beta1 may represent a new target for preventive and curative treatments of Chagas disease.
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