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A p-value greater than 0.05 indicated that the association of proteins with EC was not due to linkage disequilibrium, suggesting no significant association

only 5 out of the 21 who completed behavior assessments in the placebo group ( p = 0.03)

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Moreover, cardiomyocyte-specific knockdown of HADHA exacerbated cardiac dysfunction in mice, whereas treatment with Fer-1, an inhibitor of ferroptosis, effectively rescued cardiac function, supporting the conclusion that HADHA deficiency promotes ferroptosis predominantly through reactive oxygen species accumulation and glutathione depletion

C.YamanI.LiY.ChakravartyK.et al