Artur Miranda


Artur Miranda’s work with Chagas disease is, at the same time, to understand the parasite’s replication processes and optimize symptomatic treatment for the host. With strong family encouragement, Artur always had academia and technological innovation as his professional horizon. Artur graduated in biological sciences from the Federal University of Minas Gerais (UFMG) and has a master’s and doctorate in biochemistry and immunology from the same institution. The University of Western Ontario, in Canada, hosted a sandwich period during his doctorate. Artur also completed a postdoctoral period at the Federal University of São Paulo.

Currently a professor at the Department of Biophysics and Physiology at UFMG, science still plays a large part in his life, even outside the laboratories. It integrates his hobbies: Artur combines his interest in aquarium farming with his knowledge of electronics and carpentry to create customized homes for the fish. Furthermore, the scientist is dedicated to his passion for bodybuilding and the study of sports nutrition. His commitment to health marks his career; he is even married to a researcher who is also in the medical field. Artur’s project has the potential to impact the lives of many people affected by a disease that, unfortunately, still receives little attention.


Is the CAMKII pathway a central regulator of cardiomyocyte dysfunction and T. cruzi parasite load during the implementation of chagasic cardiomyopathy?
Science / Life Sciences

Chagas disease is caused by the parasite Trypanosoma cruzi and was initially studied by Brazilian researcher Carlos Chagas. Patients with the disease can develop gastrointestinal and especially cardiac problems, which, when present, can become very debilitating. Our research group has dedicated itself over the last decade to identifying cellular aspects of the parasite and host cells that determine the development of the cardiac form of the disease, the most serious. In this proposal, we seek to answer questions such as: is the CAMKII pathway a central regulator of cardiomyocyte dysfunction and the parasitic load of T. cruzi during the implementation of chagasic cardiomyopathy? We aim to simultaneously attenuate parasite replication and prevent/treat severe host symptoms. The success of our proposal will substantially change the treatment for Chagas disease, which is still limited, optimizing healthcare costs and improving the quality of life of those affected.

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Chamada 6