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When the GSH-dependent lipid peroxide repair system is damaged, it causes ferroptosis through the fatal accumulation of lipid-reactive oxygen species [20, 41,42,43]
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For example, the signals of high-mobility group box 1 (HMGB1), one of prototypical DAMPs released by ferroptotic cells, can be integrated by advanced glycosylation end-product specific receptor (AGER) to trigger inflammation and amplify immune responses (55)
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