ArticleFrontiers in cellular neuroscience2026
Microglial histone deacetylase-3 conditional deletion attenuates neurological deficits after intracerebral hemorrhage.
Article in Frontiers in cellular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Failed resolution of inflammation in intracerebral haemorrhage.Nature reviews. Neurology · 2026Review
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3 authors.
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Abstract
Stimulation of the innate immune system after intracerebral hemorrhage (ICH), characterized by microglial activation, contributes to ICH-induced neuroinflammation and brain damage. Despite the efficacy of broad-spectrum histone deacetylase (HDAC) inhibitors in improving acute neurological outcomes after ICH, the isoform- or cell-specific roles of histone deacetylases (HDACs) after ICH remain largely understudied. Given the emerging role of HDAC3 in various neuropathological conditions, we herein evaluate the functional role of microglial HDAC3 after ICH using newly developed microglia-specific HDAC3 conditional knockout mice (cKO). The microglia-specific conditional deletion of HDAC3 in male and female mice improved acute and long-term neurobehavioral outcomes following ICH. Furthermore, conditional deletion of HDAC3 in microglia significantly attenuated the expression of proinflammatory mediators, such as
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