Evidence map›Paper›PMID 28326018›Full record

ArticleFrontiers in cellular neuroscience2017

Neuronal Nitric Oxide Synthase in Neural Stem Cells Induces Neuronal Fate Commitment via the Inhibition of Histone Deacetylase 2.

Xing Jin, Zhang-Feng Yu, Fang Chen, Guang-Xian Lu, Xin-Yuan Ding, Lin-Jun Xie, Jian-Tong Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. The Emerging Role of the DDAH Proteins in Psychiatric Disorders.Biological psychiatry global open science · 2025
    Review
  3. Novel neurotherapeutic targets for substance use disorders: Neuroplasticity, neuroinflammation, gasotransmitters and non-canonical organ systems.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 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

7 authors at 2 institutions in 1 country.

Xing JinDepartment of Pharmacy, the Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China.
Zhang-Feng YuDepartment of Critical Care Medicine, the Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China.
Fang ChenDepartment of Pharmacy, the Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China.
Guang-Xian LuDepartment of Pharmacy, the Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China.
Xin-Yuan DingDepartment of Pharmacy, the Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China.
Lin-Jun XieDepartment of Pharmacy, the Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China.
Jian-Tong SunDepartment of Pharmacy, the Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China.
Nanjing Medical University · CNSuzhou Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Active adult neurogenesis produces new functional neurons, which replace the lost ones and contribute to brain repair. Promoting neurogenesis may offer a therapeutic strategy for human diseases associated with neurodegeneration. Here, we report that endogenous neuronal nitric oxide synthase (nNOS) for neural stem cells (NSCs) or progenitors positively regulates neurogenesis. nNOS repression exhibits significantly decreased neuronal differentiation and nNOS upregulation promotes neurons production from NSCs. Using a quantitative approach, we show that instructive effect, that is instruction of NSCs to adopt a neuronal fate, contributes to the favorable effect of endogenous nNOS on neurogenesis. Furthermore, nNOS-mediated instruction of neuronal fate commitment is predominantly due to the reduction of histone deacetylase 2 (HDAC2) expression and enzymatic activity. Further investigation will be needed to test whether HDAC2 can serve as a new target for therapeutic intervention of neurodegenerative disorders.

Indexed as

differentiationhistone deacetylase 2neural stem cellsneurogenesisneuronal nitric oxide synthase

Identifiers

PMID28326018
PMCPMC5339248
OpenAlexW2592833639

What Socratic 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 Socratic graph.