Evidence map›Paper›PMID 34381129›Full record

ArticleScientific reports2021

HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis.

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

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  13. Molecular Mechanisms of Medicinal PlantCurrent pharmaceutical design · 2024
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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

9 authors at 5 institutions in 1 country.

Jui-Sheng ChenGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Hao-Kuang WangDepartment of Neurosurgery, E-Da Hospital, Kaohsiung, Taiwan.
Chien-Yu HsuDepartment of Neurosurgery, E-Da Hospital, Kaohsiung, Taiwan.
Yu-Ting SuDepartment of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Jia-Shing ChenSchool of Medicine for International Students, College of Medicine, I-Shou University, Kaohsiung, Taiwan.
Cheng-Loong LiangDepartment of Neurosurgery, E-Da Hospital, Kaohsiung, Taiwan.
Patrick Ching-Ho HsiehInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Cheng-Chun WuSchool of Medicine, College of Medicine, I-Shou University, Kaohsiung, Taiwan. chengchunwu@isu.edu.tw.
Aij-Lie KwanGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. a_lkwan@yahoo.com.
E-Da Hospital · TWInstitute of Biomedical Sciences, Academia Sinica · TWI-Shou University · TWKaohsiung Chang Gung Memorial Hospital · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is a common cause of death worldwide and leads to disability and cognitive dysfunction. Ischemic stroke and hemorrhagic stroke are major categories of stroke, accounting for 68% and 32% of strokes, respectively. Each year, 15 million people experience stroke worldwide, and the stroke incidence is rising. Epigenetic modifications regulate gene transcription and play a major role in stroke. Accordingly, histone deacetylase 1 (HDAC1) participates in DNA damage repair and cell survival. However, the mechanisms underlying the role of HDAC1 in stroke pathogenesis are still controversial. Therefore, we investigated the role of HDAC1 in stroke by using a rat model of endothelin-1-induced brain ischemia. Our results revealed that HDAC1 was deregulated following stroke, and its expressional level and enzymatic activity were decreased. We also used MS-275 to inhibit HDAC1 function in rats exposed to ischemic insult. We found that HDAC1 inhibition promoted the infarct volume, neuronal loss, DNA damage, neuronal apoptosis after stroke, and levels of reactive oxygen species and inflammation cytokines. Additionally, HDAC1 inhibition deteriorated the behavioral outcomes of rats with ischemic insult. Overall, our findings demonstrate that HDAC1 participates in ischemic pathogenesis in the brain and possesses potential for use as a therapeutic target.

Indexed as

AnimalsApoptosisBrainBrain IschemiaCell SurvivalDNA DamageDNA RepairEpigenesis, GeneticHistone Deacetylase 1InflammationMaleNeuronsRatsRats, Sprague-DawleyStrokeHdac1 protein, ratHistone Deacetylase 1

Identifiers

PMID34381129
PMCPMC8357973
OpenAlexW3192046679

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.