Molecular mechanisms of cardiac electromechanical remodeling during Chagas disease: Role of TNF and TGF-β.
Chagas disease is caused by the trypanosomatid Trypanosoma cruzi, which chronically causes heart problems in up to 30% of infected patients. Chagas disease was initially restricted to Latin America. However, due to migratory events, this disease may become a serious worldwide health problem. During Chagas disease, many patients die of cardiac arrhythmia despite the apparent benefits of anti-arrhythmic therapy (e.g., amiodarone). Here, we assimilate the cardiac form of Chagas disease to an inflammatory cardiac disease. Evidence from the literature, mostly provided using experimental models, supports this view and argues in favor of new strategies for treating cardiac arrhythmias in Chagas disease by modulating cytokine production and/or action. But the complex nature of myocardial inflammation underlies the need to better understand the molecular mechanisms of the inflammatory response during Chagas disease. Here, particular attention has been paid to tumor necrosis factor alpha (TNF) and transforming growth factor beta (TGF-β) although other cytokines may be involved in the chagasic cardiomyopathy.
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Pampulha, Minas Gerais, Brazil.
Jader Santos
JS
Cruz
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Pampulha, Minas Gerais, Brazil.
Fabiana Simão
FS
Machado
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Pampulha, Minas Gerais, Brazil.
Catherine
C
Ropert
Laboratório de Biofísica, Departamento de Biofísica, Universidade Federal de São Paulo, Rua Botucatu, 862, Edificio de Ciências Biomédicas, 2nd Floor, Vila Clementino, 04023062 São Paulo, SP, Brazil. Electronic address: drcampos@unifesp.br.
Danilo
D
Roman-Campos
D000200:Action Potentials; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D064752:Atrial Remodeling; D002598:Chagas Cardiomyopathy / Q000188:drug therapy / Q000378:metabolism* / Q000469:parasitology / Q000503:physiopathology; D006329:Heart Conduction System / Q000187:drug effects / Q000378:metabolism* / Q000469:parasitology / Q000503:physiopathology; D006339:Heart Rate; D054884:Host-Pathogen Interactions; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009200:Myocardial Contraction; D009205:Myocarditis / Q000188:drug therapy / Q000378:metabolism* / Q000469:parasitology / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism* / Q000469:parasitology; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D014349:Trypanosoma cruzi / Q000472:pathogenicity*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism*; D020257:Ventricular Remodeling
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha
Action potential; Cardiac electrophysiology; Chagas disease; Cytokine; Trypanosoma cruzi; Tumor necrosis factor