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HDAC9 is overexpressed in neurons during stroke and exerts neurotoxic effects by inhibiting autophagy, activating inhibitor kappa B alpha /nuclear factor kappaB (IB/NFb) and mitogenactivated protein kinases (MAPKs) signaling pathways, and reducing the expression of miR20a, upregulating its target gene Neurod1 [87, 88, 89]

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