FIGURE 5.

Schematic illustration of the hypothetical positive feedback explaining the concept of oxidative inflammation. Reactive oxygen species (ROS) overproduced by oxidative stress play a central role in this vicious cycle. ROS-injured cellular components trigger systemic inflammation via activation of transcriptional factors such as nuclear factor κ-B (NFκ-B). Inflammatory endothelial dysfunction impairs erythrocyte deformability. Further, ROS-impaired erythrocyte deformability disturbs microcirculation and causes tissue hypoxia, and reoxygenation promotes overproduction of ROS and imbalance of redox homeostasis. Redox-sensitive NF-κB activation sustains systemic inflammation, and inflamed immune cells generate ROS maintaining the putative positive feedback.