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Mechanistically, OXNAD1 directly bound to and suppressed the ferroptosis driver PTGS2, thereby attenuating lipid peroxidation and mitochondrial damage, ultimately restraining ferroptosis and promoting drug resistance

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In different types of tissues, including the human fetal tissues, PR-B has been widely associated with higher transcriptional activity, whereas PR-A has more transcription-inhibitory effects, particularly on the PR-B, ER, and GR (72)