The Role of Dystrophin Loss in the Trypanosoma cruzi Infection

Dystrophin, an important protein of the dystrophin-glycoprotein complex, has been implicated in the pathogenesis of experimental Chagas disease. It contributes to cell shape, mechanical resistance, contraction and force generation in cardiomyocytes. Dystrophin loss has been associated with end-stage cardiomyopathies and proposed as a common route for myocardial dysfunction and progression to advanced heart failure. One of the most intriguing aspects of chronic Chagasic cardiomyopathy is the long delay after the initial infection to the cardiac manifestations. This has been partially explained by our group in previous studies demonstrating loss/reduction of dystrophin in mice experimentally infected with T. cruzi. The analysis of dystrophin expression showed significant reduction in the acute phase, with the reduction maintained up to the chronic phase. Inflammatory mechanisms could be involved in the dystrophin loss since inflammation has been shown to play a key role in the activation of proteases responsible for dystrophin degradation.