Evidence map›Paper›PMID 26338677›Full record

ArticleTranslational stroke research2016

The Histone Deacetylase Inhibitor Suberoylanilide Hydroxamic Acid (SAHA) Confers Acute Neuroprotection After Intracerebral Hemorrhage in Mice.

Sangeetha Sukumari-Ramesh, Cargill H Alleyne, Krishnan M Dhandapani

Abstract read
PubMed Publisher
In one paragraph

Article in Translational stroke research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  15. HDAC inhibition reduces white matter injury after intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  16. Article
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  18. Revisiting promising preclinical intracerebral hemorrhage studies to highlight repurposable drugs for translation.International journal of stroke : official journal of the International Stroke Society · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Sangeetha Sukumari-RameshDepartment of Neurosurgery, Georgia Regents University, 1120 15th Street CA1010, Augusta, GA, 30912, USA. sramesh@gru.edu.
Cargill H AlleyneDepartment of Neurosurgery, Georgia Regents University, 1120 15th Street CA1010, Augusta, GA, 30912, USA.
Krishnan M DhandapaniDepartment of Neurosurgery, Georgia Regents University, 1120 15th Street CA1010, Augusta, GA, 30912, USA.
Augusta University · USGeorgia Regents Medical Center · US

Funding

HMGB1 and Traumatic Brain InjuryR01NS065172 · NINDS · AUGUSTA UNIVERSITY · PI DHANDAPANI, KRISHNAN M. · 2009 to 2013
$1.6M
Therapeutic targeting of CD36 after intracerebral hemorrhageR21NS075774 · NINDS · AUGUSTA UNIVERSITY · PI DHANDAPANI, KRISHNAN M. · 2012 to 2013
$368k
NINDS NIH HHS R01NS065172NINDS NIH HHS R21NS075774
6 · The paper itself

Abstract

Spontaneous intracerebral hemorrhage (ICH) is a stroke subtype with no effective treatment. Though ICH is known to induce severe neurological damage, the molecular mechanisms of neurological injury after ICH remain largely unclear. Given the emerging role of epigenetic mechanisms in neurodegeneration, the present study evaluated whether suberoylanilide hydroxamic acid (SAHA: vorinostat), a clinically well-tolerated pan-histone deacetylase inhibitor (HDACi), would attenuate neurological injury and improve functional outcomes in a preclinical model of ICH. Mice were administered with SAHA or vehicle after an induction of ICH and acute neuronal death, glial activation, and neurological outcomes were assessed. SAHA-treated mice exhibited less neurodegeneration with concomitant improvement in neurological outcomes than vehicle-treated mice. Furthermore, SAHA downregulated glial activation and the expression of heme oxygenase-1, a stress-inducible enzyme that plays critical roles in neurological damage after ICH. Altogether, the data strongly suggest the role of epigenetic mechanisms in inducing neurological injury after ICH and raise the possible clinical utility of SAHA for therapeutic intervention after ICH.

Indexed as

AnimalsBrainBrain InjuriesCerebral HemorrhageDisease Models, AnimalFluoresceinsGlial Fibrillary Acidic ProteinHeme Oxygenase-1Histone Deacetylase InhibitorsHydroxamic AcidsIn Situ Nick-End LabelingMaleMembrane ProteinsMiceNeurologic ExaminationVorinostatFluoresceinsfluoro jadeGlial Fibrillary Acidic ProteinHeme Oxygenase-1Histone Deacetylase InhibitorsHmox1 protein, mouseHydroxamic AcidsMembrane ProteinsVorinostatGliosisMicroglial activationStroke

Identifiers

PMID26338677
OpenAlexW1889589868

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.