Evidence map›Paper›PMID 34638996›Full record

ArticleInternational journal of molecular sciences2021

Restoration of HDAC1 Enzymatic Activity after Stroke Protects Neurons from Ischemia/Reperfusion Damage and Attenuates Behavioral Deficits in Rats.

Jui-Sheng Chen, Hao-Kuang Wang, Yu-Ting Su, Chien-Yu Hsu, Jia-Shing Chen, Cheng-Loong Liang, Cheng-Chun Wu, Aij-Lie Kwan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
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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

8 authors at 3 institutions in 1 country.

Jui-Sheng ChenGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.ORCID 0000-0001-7627-6132
Hao-Kuang WangDepartment of Neurosurgery, E-DA Hospital, I-Shou University, Kaohsiung 824, Taiwan.ORCID 0000-0002-1928-7502
Yu-Ting SuDepartment of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
Chien-Yu HsuDepartment of Neurosurgery, E-DA Hospital, I-Shou University, Kaohsiung 824, Taiwan.
Jia-Shing ChenSchool of Medicine for International Students, College of Medicine, I-Shou University, Kaohsiung 824, Taiwan.
Cheng-Loong LiangDepartment of Neurosurgery, E-DA Hospital, I-Shou University, Kaohsiung 824, Taiwan.
Cheng-Chun WuSchool of Medicine, College of Medicine, I-Shou University, Kaohsiung 824, Taiwan.ORCID 0000-0002-7084-9208
Aij-Lie KwanGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
I-Shou University · TWKaohsiung Medical University · TWChang Gung University · TW

Funding

E-Da Hospital EDAHP108025, EDAH109029, EDAH109039, EDAHP110001, EDAHP110032, EDAHS109003I-Shou University ISU-110-IUC-07, ISU 110-S-01Ministry of Science and Technology, Taiwan 109-2320-B-214-001
6 · The paper itself

Abstract

A therapeutic approach for promoting neuroprotection and brain functional regeneration after strokes is still lacking. Histone deacetylase 1 (HDAC1), which belongs to the histone deacetylase family, is involved in the transcriptional repression of cell-cycle-modulated genes and DNA damage repair during neurodegeneration. Our previous data showed that the protein level and enzymatic activity of HDAC1 are deregulated in stroke pathogenesis. A novel compound named 5104434 exhibits efficacy to selectively activate HDAC1 enzymatic function in neurodegeneration, but its potential in stroke therapy is still unknown. In this study, we adopted an induced rat model with cerebral ischemia using the vessel dilator endothelin-1 to evaluate the potential of compound 5104434. Our results indicated compound 5104434 selectively restored HDAC1 enzymatic activity after oxygen and glucose deprivation, preserved neurite morphology, and protected neurons from ischemic damage in vitro. In addition, compound 5104434 attenuated the infarct volume, neuronal loss, apoptosis, DNA damage, and DNA breaks in cerebral ischemia rats. It further ameliorated the behavioral outcomes of neuromuscular response, balance, forepaw strength, and functional recovery. Collectively, our data support the efficacy of compound 5104434 in stroke therapy and contend that it can be considered for clinical trial evaluation.

Indexed as

AnimalsApoptosisBehavior, AnimalBrain IschemiaDisease Models, AnimalDNA DamageEnzyme ActivationEnzyme ActivatorsFemaleHistone Deacetylase 1MaleMuscle StrengthNeuronsPostural BalanceProtective AgentsRatsEnzyme ActivatorsHdac1 protein, ratHistone Deacetylase 1Protective Agentsapoptosiscylinder testDNA damageHDAC1mNSSstroke

Identifiers

PMID34638996
PMCPMC8508747
OpenAlexW3201712849

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.