ArticleAnnals of medicine2025
HDAC1 dysregulation promotes pro-inflammatory microglial activation and aggravates post-stroke neuroinflammation.
Article in Annals of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- From oxidative stress to epigenetic regulation: Molecular mechanisms of preterm brain injury and neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Clinical value of LncRNA PAX8-AS1 as a biomarker for sepsis diagnosis and prognosis and its regulatory mechanism via the miR-34a-5p/HDAC1 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- IL-10-STAT3-Dependent Transcriptional Regulation in Microglia: Alzheimer's Disease and Neuroinflammation.Biomedicines · 2026Review
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
backgroundHistone deacetylase 1 (HDAC1) is a key epigenetic regulator involved in DNA repair and neuronal survival. While HDAC1 downregulation has been implicated in ischemic brain injury, its role in regulating microglial functional shift and neuroinflammation remains unclear. This study aimed to investigate how HDAC1 dysfunction influences microglial activation states and contributes to neuroinflammatory processes in ischemic stroke.
methodsUsing a rat model of endothelin-1-induced focal cerebral ischemia, HDAC1 knockdown was achieved
resultsHDAC1 knockdown
conclusionHDAC1 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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Registered trials
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