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Considerable progress has been made toward developing new drugs for ferroptosis, utilizing the well-known targets of the pathological conditions (160, 161)

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As expected from our previous experiments, the P44A mutant precipitated slower than the WT in the presence of EGCG, although the effect was not as pronounced as in the solid-state NMR experiments reported above

These findings indicate that inflammatory conditions associated with the overactivation of NF-B may misalign the molecular clock, thereby altering the transcription of several target genes and contributing to metabolic inflammation through direct transcriptional reprogramming