The Oxidative Stress and Chronic Inflammatory Process in Chagas Disease: Role of Exosomes and Contributing Genetic Factors

Figure 2

The persisting ROS signal activates proinflammatory gene expression. T. cruzi-infected cardiomyocytes are able to produce mtROS, which induces the dissociation of NF-κB transcription factor from IκB in the cytoplasm and translocate to the nucleus to bind target sequences in the gene promoter of proinflammatory cytokine genes, which leads to the high production of proinflammatory cytokines, which in turn can produce tissue damage. Mitochondrial ROS can produce DNA damage and activate PARP1 to produce PAR, which signals transcriptional coactivators to induce proinflammatory cytokine gene expression and modify histones at the gene promoter regions. Alternatively, ROS could activate an epigenetic modification system (EMS) that might be able to produce an epigenetic modification (EM) at the promoter regions of proinflammatory cytokine genes to keep them in an active transcribing state, even though in the absence of T. cruzi. +1 represents the transcription start site of the genes.