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Although iron-dependent prolyl hydroxylases (PHDs) regulate both isoforms and iron chelation can stabilize HIF-1 and HIF-2 in vitro (74), these observations collectively suggest that the gut may implement additional, tissue-specific mechanisms that bias HIF isoform activity and downstream iron handling

coli is a familiar commensal bacterium that colonizes the gut soon after birth

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This limitation has stimulated interest in targeted antiferroptotic approaches that aim to interrupt this pathological cycle and promote tissue repair