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Chagasic cardiomyopathy (CCC) is a very intriguing biological problem. CCC occurs in a scenario of disrupted calcium handling and enhanced oxidative stress, which combined, may favor the hyper activation of calcium/calmodulin-dependent protein kinase II (CaMKII) signaling pathway and the production of reactive oxygen species, which per se is fundamental for heart physiology. Our group has been evaluating the association between CaMKII signaling in the electro-mechanical (dys)function of the heart in early stages of chronic experimental Chagas disease. We observed that inhibition of CaMKII axis reversed the pro-arrhythmic profile of isolated hearts and isolated cardiomyocytes. The benefits of the limited CaMKII activation to the electrical properties of cardiomyocytes are co-related to the restoration of Ca2+ handling in a damaged cellular environment created after T. cruzi infection. The role of reactive oxygen species will be discussed.
This work was supported by Conselho Nac. Des. Cient. Tecnologico (CNPq #437969/2018-5, #312474/2017-2 and #312939/2021-3) and by the Fundação de Amparo à Pesquisa do Estado de São Paulo e de Minas Gerais (FAPESP e FAPEMIG).
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