Research reveals hdac1's role in worsening neuroinflammation and neuronal injury after ischaemic stroke, suggesting it as a target for treatment.
HDAC1 acts as a key repressor of NF-κB-driven pro-inflammatory microglial activation and neuroinflammation in stroke. Its loss exacerbates inflammatory cascades, immune cell infiltration, and neuronal injury, underscoring HDAC1 as a potential therapeutic target for limiting secondary brain damage after ischaemic stroke.
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Chen et al. (2025) studied this question.
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