Evidence map›Paper›PMID 28656275›Full record

ArticleMolecular medicine reports2017

Histone deacetylase-2 is involved in stress-induced cognitive impairment via histone deacetylation and PI3K/AKT signaling pathway modification.

Jie Wu, Cui Liu, Ling Zhang, Chun-Hui Qu, Xiao-Long Sui, Hua Zhu, Lan Huang, Yan-Feng Xu, Yun-Lin Han, Chuan Qin

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Role of epigenetic regulation in diminished ovarian reserve.Journal of assisted reproduction and genetics · 2025
    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

10 authors at 2 institutions in 1 country.

Jie WuInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Cui LiuInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Ling ZhangInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Chun-Hui QuInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Xiao-Long SuiInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Hua ZhuInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Lan HuangInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Yan-Feng XuInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Yun-Lin HanInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Chuan QinInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P.R. China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNInstitute of Laboratory Animal Science · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to chronic stress upregulates blood glucocorticoid levels and impairs cognition via diverse epigenetic mechanisms, such as histone deacetylation. Histone deacetylation can lead to transcriptional silencing of many proteins involved in cognition and may also cause learning and memory dysfunction. Histone deacetylase‑2 (HDAC2) has been demonstrated to epigenetically block cognition via a reduction in the histone acetylation level; however, it is unknown whether HDAC2 is involved in the cognitive decline induced by chronic stress. To the best of authors' knowledge, this is the first study to demonstrate that the stress hormone corticosteroid upregulate HDAC2 protein levels in neuro‑2a cells and cause cell injuries. HDAC2 knockdown resulted in a significant amelioration of the pathological changes in N2a cells via the upregulation of histone acetylation and modifications in the phosphoinositide 3‑kinase/protein kinase B signaling pathway. In addition, the HDAC2 protein levels were upregulated in 12‑month‑old female C57BL/6J mice under chronic stress in vivo. Taken together, these findings suggested that HDAC2 may be an important negative regulator involved in chronic stress‑induced cognitive impairment.

Indexed as

Signal TransductionStress, PhysiologicalAcetylationAdrenal Cortex HormonesAnimalsCell Line, TumorCell SurvivalCognitive DysfunctionFemaleGene Knockdown TechniquesHistone Deacetylase 2HistonesLentivirusMice, Inbred C57BLNeuronal OutgrowthPhosphatidylinositol 3-KinasesAdrenal Cortex HormonesHistone Deacetylase 2HistonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID28656275
PMCPMC5561802
OpenAlexW2670091564

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.