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This regulatory relationship is inversely validated at the molecular level: the GPX4 inhibitor RSL3 potently induces ferroptosis by binding to its active site, serving as a reliable experimental tool for studying ferroptosis in AD and directly establishing a causal link between GPX4 inhibition and AD pathology (191)

66 In contrast, preserving GSH by supplementing cysteine or GSH precursors helps bacteria survive oxidative challenge

4a, excessive accumulation of ROS triggers KEAP1 activation and enables KEAP1 to interact with PGAM5

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