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Under oxidative stress and induced by excessive ROS generation, Nrf2 is released from its inhibitor Keap1, allowing its translocation into the nucleus (Kasprzak et al., 2020), where it binds to the antioxidant response element (ARE) present in the DNA sequence of numerous antioxidant enzymes like glutathione-S-transferase, -glutamyl cysteine synthetase (glutamate cysteine ligase), heme oxygenase 1, and paraoxonase-1 inducing their transcription, managing the phase II response to oxidative stress (Kasprzak et al., 2020)

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However, when cellular metabolism is dysregulated (e.g., through excessive iron accumulation or hyperactive mitochondrial metabolism), this oxidative/antioxidant balance is disrupted

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