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The onset of ferroptosis is primarily attributed to the effects of ferroptosis-promoting factors or prerequisites outweighing the cellular antioxidant mechanisms and defensive systems against ferroptosis
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Animal studies have confirmed that various oxidative stresses can induce the release of highly acetylated HMGB1 under various pathological conditions The translocation of Cathepsin B from the lysosome to the nucleus induces DNA damage, leading to the subsequent release of HMGB1, which can induce the occurrence of ferroptosis[136]
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