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Graphic abstract. DYRK1A phosphorylates WDR82 and KAT6A to reduce deposition of H3K4me3 and H3K27ac on the promoters of cell cycle genes, thereby limiting their transcriptional activation and inhibiting cardiomyocyte cell cycle activity. Either pharmacological inhibition or genetic deletion of DYRK1A promotes cardiomyocyte cell cycle activation and cardiac repair in adult heart post-MI.
