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Unlike the positive influence of most indole derivatives in the gut, IAA, indoxyl sulfate, and indoxyl-β-D-glucuronide act in cells of the cardiovascular system as pathogenic agents that, via the AHR, induce the transcription of proinflammatory cytokines, apoptosis, and oxidative stress
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These results indicate that ACE at therapeutic doses has no significant risk of ferroptosis induction in normal tissues and that the clinical application of ACE provides a solid basis for translational medicine
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