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The cited pharmacological study has demonstrated that curdione modulates redox complexes by disrupting Keap1-Trx1 interactions while enhancing Trx1-GPX4 binding, thereby attenuating post-infarction ferroptosis through Keap1/Trx1/GPX4 axis regulation (64)

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In comparison to healthy controls, ARDS patients exhibited significantly different plasma PC compositions, with an overall increase in methyl-D9-PC enrichment but considerably lower enrichment of methyl-D3-PC and methyl-D6-PC, indicating significant changes in the PC synthesis pathway in ARDS patients