Regulation of cellular redox homeostasis determines the fate of the cell. Perturbation in redox status is known to elicit multiple cellular pathways. Role of oxidative stress modulation in channelizing the cell towards apoptosis or rescuing the cell by activating pro-survival pathways, depends on the levels of generated oxidative stress. High levels of generated oxidative stress induce cell death pathways whereas mild and low levels are known to elicit the cell survival pathways. Generation of ROS for a short duration of time inducing Redox ticking also triggers the pro-survival pathways inside the cell. Nrf2 is the redox sensitive prosurvival transcription factor which acts as master regulator of redox equilibrium. Nrf2 and its dependent genes including HO-1, GCLC, NQO1 etc. are involved in maintaining the cellular redox homeostasis. Role of Nrf2 as dual edges sword has been highlighted in past decade. The cross talk between the Nrf2 and NF-κB is at the focal point of building the redox response network. The present chapter is aimed at providing the insight on the role of Nrf2 and NF-κB as redox sensitive transcription factors in regulating cellular redox status. Further, the chapter brings in light the therapeutic potential of targeting Nrf2 under multiple clinical settings.
Part of the book: Reactive Oxygen Species