Abstract
The KEAP1-NRF2 axis is pivotal in the cellular mechanism against oxidative and electrophilic stress. NRF2, under standard conditions, undergoes proteasomal degradation mediated by the E3 ubiquitin ligase KEAP1. Stress conditions lead to KEAP1 inactivation, facilitating NRF2 stability and subsequent activation of defensive genes. NRF2 signaling anomalies are associated with cancer progression and neurodegenerative diseases. Continuous activation of the NRF2 pathway aids in the survival of cancer cells, while a deficiency in NRF2 functionality intensifies inflammation and oxidative injury in neurodegenerative disease models. Thus, the modulation of this pathway is being investigated for therapeutic applications in both cancer and neurodegenerative diseases.