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This difference in metabolic alterations in response to riboflavin deficiency is consistent with our previous findings in absence of Rtbdn showing separate metabolic priorities for the NR and RPE, especially when measuring steady state levels of metabolites [12]

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Importantly, in our previous research, we found that SIRT1 knockdown mice ( SIRT1 +/- mice) exhibits significant pre-eclampsia-like performances, such as hypertension, proteinuria, fetal growth restriction, kidney injury, and narrow labyrinthine layer, while the manifestations could be reversed after intraperitoneally injecting SRT2104, which is a highly selective agonist of SIRT1[17]