ArticleJournal of the American Heart Association2017
Inhibiting Histone Deacetylase 2 (HDAC2) Promotes Functional Recovery From Stroke.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.
- Role of histone deacetylases and sirtuins in the ischaemic stroke: a systematic review and meta-analysis of animal studies.Stroke and vascular neurology · 2026Pooled it
- The Role of Genetics in Stroke Risk and Outcome: A Review of Current Evidence.Brain and behavior · 2025Pooled it
- A Voxel-Wise T2 Distribution Framework for Lesion Severity Stratification and Treatment-Response Assessment in Stroke: Insights Into Suberoylanilide Hydroxamic Acid-Induced Neuroprotection.Magnetic resonance in medicine · 2026Article
- Nonexpansive biodegradable matrix promotes blood vessel organoid development for neurovascular repair and functional recovery in ischaemic stroke.Nature biomedical engineering · 2026Article
- Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- An Epigenetic Switch for Sex-Specific Brain Resilience in Stroke: Targeting HDAC2 to Amplify Endogenous Oxytocin Signaling.ACS central science · 2026Article
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- Epigenetic Regulation in Ischemic Neuroprotection: The Dual Role of HDACs and HATs in Neuroinflammation and Recovery.Antioxidants (Basel, Switzerland) · 2025Review
- Molecular Mediators of Neutrophil Primary Granule Release Following Acute Ischemic Stroke and their Associated Epigenetic Modulation by HDAC2.Molecular neurobiology · 2025Article
- Environmental enrichment: a neurostimulatory approach to aging and ischemic stroke recovery and rehabilitation.Biogerontology · 2025Review
- Potential therapeutic targets for ischemic stroke in pre-clinical studies: Epigenetic-modifying enzymes DNMT/TET and HAT/HDAC.Frontiers in pharmacology · 2025Review
- S-Nitrosylation of Dexras1 Controls Post-Stroke Recovery via Regulation of Neuronal Excitability and Dendritic Remodeling.CNS neuroscience & therapeutics · 2025Article
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- Inhibition of OGFOD1 by FG4592 confers neuroprotection by activating unfolded protein response and autophagy after ischemic stroke.Journal of translational medicine · 2024Article
- nNOS and Neurological, Neuropsychiatric Disorders: A 20-Year Story.Neuroscience bulletin · 2023Review
- Reactivation of corticogenesis-related transcriptional factors BCL11B and SATB2 after ischemic lesion of the adult mouse brain.Scientific reports · 2023Article
- Ketogenic Diet and Ketone Bodies against Ischemic Injury: Targets, Mechanisms, and Therapeutic Potential.International journal of molecular sciences · 2023Review
- Male histone deacetylase 6 (HDAC6) knockout mice have enhanced ventilatory responses to hypoxic challenge.Frontiers in physiology · 2023Article
- Epigenetic mechanisms and potential therapeutic targets in stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- Advancement of epigenetics in stroke.Frontiers in neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStroke is a leading cause of long-term disability worldwide. However, current therapies that promote functional recovery from stroke are limited to physical rehabilitation. No pharmacological therapy is available. Thus, understanding the role of histone deacetylase 2 (HDAC2) in the pathophysiological process of stroke-induced functional loss may provide a novel strategy for stroke recovery. METHODS AND
resultsFocal stroke was induced by photothrombosis. LV-HDAC2-shRNA-GFP, LV-GFP, Ad-HDAC2-Flag, or Ad-inactive-HDAC2-Flag was microinjected into the peri-infarct area immediately after stroke. HDAC inhibitors were microinjected into the peri-infarct area 4 to 10 days after stroke. Grid-walking task and cylinder task were conducted to assess motor function. Golgi-Cox staining, chromatin immunoprecipitation, and electrophysiology were used to reveal the mechanisms underlying stroke recovery. Knockdown or knockout of HDAC2 promoted stroke recovery, whereas overexpression of HDAC2 worsened stroke-induced functional impairment. More importantly, trichostatin A, a pan-HDAC inhibitor, promoted functional recovery from stroke in WT mice when used in the delayed phase, but it was ineffective in
conclusionsOur novel findings provide evidence that HDAC2 is a crucial target for functional recovery from stroke. As there are clinically available HDAC inhibitors, our findings could be directly translated into clinical research of stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.