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Therefore, the future of ferroptosis-targeted therapy depends not only on discovering new inhibitors or inducers but also on solving the core issues of how to deliver the right drug to the right brain region in the right patient and how to reliably monitor ferroptosis in clinical settings

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Dysfunctional ENaCs have been implicated in Liddle syndrome, pseudohypoaldosteronism, cystic fibrosis, and may contribute to salt-sensitive hypertension [15]