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Rather than functioning as isolated antioxidant modules, these pathways form a highly interconnected redox buffering network in which compensatory capacity, metabolic flux, and iron availability collectively determine ferroptotic susceptibility
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Mechanistically, KDM3B knockdown did not change the H3K9 methylation level on the SLC7A11 promoter, while KDM3B cooperates with transcription factor ATF4 to upregulate the expression of SLC7A11
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