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Emerging evidence indicates that riboflavin deficiency skews microglia toward a pro-inflammatory M1 phenotype, characterized by elevated iNOS, IL-1, and TNF-, whereas riboflavin supplementation promotes an anti-inflammatory M2 phenotype, with higher IL-10 and TGF- expression via STAT6 activation (67, 68)

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Translation reinitiation at alternative open reading frames regulates gene expression in an integrated stress response