Instead, PARP1 depletion preserved the POLG-dependent mtDNA content, mitochondrial function, and antioxidant/oxidant balance in chagasic myocardium and human cardiomyocytes infected by T. cruzi. Taken together, we have demonstrated that the mitochondrial transport of PARP1/PAR adversely impacts the mtDNA maintenance by POLG replisome, and exacerbates the mitochondrial dysfunction, oxidative stress and cardiac remodeling in Chagas disease. The gene discussed is POLG; the disease is Chagas disease.