Evidence map›Paper›PMID 37377100›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2023

N-acetylcysteine improves autism-like behavior by recovering autophagic deficiency and decreasing Notch-1/Hes-1 pathway activity.

Ying-Hua Zhang, Ting Wang, Yan-Fang Li, Ya-Nan Deng, Xue-Ling He, Li-Jun Wang

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2023. 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
1.8field-weighted citation impact, top 16% 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, 10 citations in OpenAlex.

  1. Valproate Exposure as anCNS & neurological disorders drug targets · 2025
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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

6 authors at 1 institution in 1 country.

Ying-Hua ZhangDepartment of Human Anatomy & Histoembryology, Henan Key Laboratory of Biological Psychiatry, School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003, China.ORCID 0000-0003-3033-9980
Ting WangDepartment of Human Anatomy & Histoembryology, Henan Key Laboratory of Biological Psychiatry, School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003, China.
Yan-Fang LiDepartment of Human Anatomy & Histoembryology, Henan Key Laboratory of Biological Psychiatry, School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003, China.
Ya-Nan DengDepartment of Human Anatomy & Histoembryology, Henan Key Laboratory of Biological Psychiatry, School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003, China.
Xue-Ling HeDepartment of Human Anatomy & Histoembryology, Henan Key Laboratory of Biological Psychiatry, School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003, China.
Li-Jun WangDepartment of Human Anatomy & Histoembryology, Henan Key Laboratory of Biological Psychiatry, School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003, China.
Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-acetylcysteine (NAC) has been reported to improve social interaction behavior, irritability, self-injury, and anxiety-like behavior in autism. However, the molecular mechanism underlying the therapeutic roles of NAC in autism remains unknown. This study mainly aimed to investigate the therapeutic effect of NAC on valproic acid (VPA)-induced autism model and the underlying mechanisms. Our results showed that NAC ameliorated the deficits in sociability and the anxiety- and repetitive-like behaviors displayed by VPA-exposed rats. In addition, VPA exposure induced autophagic deficiency and enhanced Notch-1/Hes-1 pathway activity based on lowered Beclin-1 and LC3B levels, while increased expression of p62, Notch-1, and Hes-1 expression at the protein level. However, NAC recovered VPA-induced autophagic deficiency and reduced Notch-1/Hes-1 pathway activity in a VPA-exposed autism rat model and SH-SY5Y neural cells. The present results demonstrated that NAC improves autism-like behavioral abnormalities by inactivating Notch-1/Hes-1 signaling pathway and recovering autophagic deficiency. Taken together, this study helps to elucidate a novel molecular mechanism that underlies the therapeutic actions of NAC in autism and suggests its potential to ameliorate behavioral abnormalities in neurodevelopmental disorders.

Indexed as

Autistic DisorderNeuroblastomaPrenatal Exposure Delayed EffectsAcetylcysteineAnimalsBehavior, AnimalDisease Models, AnimalFemaleHumansRatsValproic AcidAcetylcysteineValproic Acidautismautophagic deficiencyHes-1N-acetylcysteineneuroscienceNotch-1 pathway

Identifiers

PMID37377100
PMCPMC10525405
OpenAlexW4382344395

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.