Molecular Mechanisms of Nrf2 in Inflammation: Interactions Between Nrf2 and Inflammatory Mediators

Inflammation is a common feature of chronic age-related diseases. Therefore, controlling inflammation by manipulation in the molecular mechanisms that cause the inflammatory process becomes critical to improve human health by preventing various diseases such as cancer, metabolic syndrome, neurodegenerative diseases, and many others. The transcription factor Nrf2 is essential for protection against oxidative/xenobiotic stress. However, Nrf2 also decreases inflammation through a cross talk with the NF kappa B signaling pathway. Although the mechanism by which Nrf2 mediates anti-inflammatory response is not fully elucidated, new insights have identified that in addition to regulating the expression of cytoprotective genes that have an established and well-known "antioxidant response element, ARE,", Nrf2 can also regulate over six hundred additional genes that do not have an ARE sequence, including genes coding for proinflammatory cytokines. In this chapter, we summarize and discuss the direct and indirect role of Nrf2 in the regulation of inflammatory response and the development of therapeutic targets by identifying new molecular mechanisms.