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Although direct evidence for these interactions was not provided in the present study, our data point to mitochondrial oxidative stress and altered cellular energy sensing pathways as key questions to tackle in future investigations of SLC25A39 deficiency

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166 A recent study reported that S-nitrosylation altered AAT to a proinflammatory protein, which facilitated the inflammatory state of macrophages by upregulating proinflammatory molecules and the activation of MAPK signalling pathways