**7. Conclusion**

Cellular redox equilibrium is pivotal for normal cellular functioning and responses. Impairment in regulation and maintenance of redox homeostasis underlines the pathogenesis of multiple associated diseases. Thus, identifying the key players in redox *Perturbation of Cellular Redox Status: Role of Nrf2, a Master Regulator of Cellular Redox DOI: http://dx.doi.org/10.5772/intechopen.102319*

regulation is of prime interest. Nrf2 and NF-KB are the two most pivotal and embroiled redox sensitive transcription factors that underlines the maintenance of redox balance. Thus, the two pathways are at the epicenter of investigation with clinical significance. The Nrf2 is the master regulator of cellular redox status. The Nrf2 and its dependent genes are responsible for cytoprotection, immunoregulation, maintaining cellular antioxidant levels, reducing drug toxicities etc. Presence of multiple critical cysteine residues in KEAP-1, inhibitor of Nrf2, renders redox sensitivity in activation of Nrf2 pathway. Aberrant expression and regulation of Nrf2 pathway has been implicated in various pathologies including cancer, diabetes, neurodegeneration etc. Multiple researchers have demonstrated the targeting of Nrf2 as key strategy to curb inflammation and associated disorders. Apart from Nrf2, another redox sensitive transcription factor is NF-κB. Aberrant activation of NF-κB pathway has been implicated in inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-κB also contains cysteine residues which act as sensors for redox modulation. Recent advances have highlighted the cross talk between Nrf2 and NF-κB as putative target for strategic drug development. Further, in depth clinically relevant exploration of the cross talk is warranted. The triangulate interplay of cellular redox, Nrf2 and NF-κB have immense potential to generate the therapeutic benefits via serving a putative target for discovering and developing novel drugs.
