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.]. We utilized fluorescence probes, biochemical and molecular assays, and cutting-edge in situ respirometry and 3-dimensional echocardiography to test our hypothesis. Our results suggest that genetic deletion or chemical inhibition of PARP1 was beneficial in improving mitochondrial health in chagasic mice. Genetic depletion or chemical inhibition of PARP1 resulted in a decline in chronic oxidative stress and cardiac remodeling, and an improvement in mitochondrial coupled respiration and LV function. We discuss the potential mechanism of PARP1/PAR interference with mitochondrial function in Chagas disease.


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