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This mechanism is particularly significant for lupus pathogenesis, given that DN T cells are a primary source of pro-inflammatory IL-4, IL-17 and necrotic debris (Lai et al

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4-hydroxynonenal self-limits Fas-mediated DISC-independent apoptosis by promoting export of Daxx from the nucleus to the cytosol and its binding to Fas

All LOX isoforms promote PUFA peroxidation, and their knockdown has been consistently shown to attenuate ferroptosis (43)