ArticleFrontiers in pharmacology2026
Retinoic acid alleviates manganese-induced neurotoxicity in SH-SY5Y cells via the Trim28/α-synuclein/H4K91ac epigenetic axis.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Manganese (Mn)-induced neurotoxicity is a major public health concern. The aim of this study is to assess whether retinoic acid, a metabolite of vitamin A, can counteract manganese-induced neurotoxicity in SH-SY5Y cells by counteracting epigenetic dysregulation. Methods: Results: Mn exposure induced behavioral deficits, synaptic damage, and dopaminergic dysfunction in rats. Mechanistically, Trim28 mediated α-syn nuclear translocation. Nuclear α-syn bound histone H4, reducing H4K91ac enrichment at the DAT promoter, suppressing DAT expression, and disrupting dopamine homeostasis. Knockdown of Trim28 or α-syn reversed these effects. Retinoic acid inhibits the nuclear translocation of α-syn by modulating Trim28, and restores the levels of H4K91ac and DAT, thereby alleviating manganese-induced neurotoxicity in cells. Conclusion: This study elucidates the role of the Trim28/α-syn/H4K91ac axis in manganese-induced dopaminergic dysfunction and identifies Trim28 as a potential target for retinoic acid.
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