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These findings suggest that the use of agents that inhibit GPX4 degradation may provide an effective means of mitigating ferroptosis-related lethal effects in IBD

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The rationale is that under normal physiological circumstances, the decline in IGFBP-1 from its maximally stimulated overnight fasting level (34) to the level seen after food intake on a molar basis is relatively modest, and only leads to minor increases in serum free IGF-I (37, 38)