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Although the exact molecular mechanism of the dual regulation of ferroptosis by butyrate has not been fully elucidated, accumulating experimental evidence gradually suggests that it may be involved in the pathophysiological regulation of OA by regulating the ferroptosis process of chondrocytes

Further epigenetic evaluation revealed reductions in three histones (H3Ac, H4Ac, H3K4me3) that transcriptionally activate insulin-2 gene promoters and significant elevation in two histones (H3K9me3, H3K20me3) that suppress/silence these promoters [172]

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