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The increased susceptibility to cell death could exaggerate inflammation via the release of damage signals (e.g., ATP, High mobility group box 1 protein (HMGB1)) or alternatively, ferroptosis of CD16 + monocytes and/or macrophages that are reputedly more pro-inflammatory than intestinal macrophages could serve to limit inflammation

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430 These findings suggest that iron metabolism is abnormal in the cells of Friedreichs Ataxia models, and regulation of iron metabolism may have some ameliorative effects on Friedreichs Ataxia

[DOI] [PubMed] [Google Scholar] McGuinness AJ, Sapey E