Abstract

Reactive oxygen species (ROS) generation is an intrinsic event that occurs during the onset of the inflammatory cascade. ROS are crucial for host defense and for the redox-dependent activation of proinflammatory mediators such as NF-κB and NLRP3 inflammasomes. Similarly, ROS can also activate antioxidant and anti-inflammatory transcription factors that control the expression of genes necessary for the resolution of inflammation and the prevention of oxidative stress. Dysregulation of ROS production or insufficient ROS scavenging, however, results in the oxidation of biomolecules and the structural modification of proteins triggering signaling cascades that lead to the onset and progression of inflammatory diseases. Peroxiredoxins regulate ROS levels and thus play a central role in redox signaling. Recent evidence suggests that peroxiredoxins can also activate proinflammatory pathways. The current knowledge of the redox signaling events that occur during the onset of inflammation is discussed in this chapter.

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