Evidence map›Paper›PMID 37078424›Full record

ArticleEMBO molecular medicine2023

Axin2 coupled excessive Wnt-glycolysis signaling mediates social defect in autism spectrum disorders.

Mengmeng Wang, Panpan Xian, Weian Zheng, Zhenzhen Li, Andi Chen, Haoxiang Xiao, Chao Xu, Fei Wang, Honghui Mao, Han Meng and 4 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Mengmeng Wang *Department of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Panpan Xian *Department of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Weian Zheng *Department of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Zhenzhen LiDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Andi ChenDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Haoxiang XiaoDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Chao XuDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-5471-7555
Fei WangDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Honghui MaoDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-5625-3715
Han MengDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-7555-3174
Youyi ZhaoState Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases and Shaanxi Engineering Research, Center for Dental Materials and Advanced Manufacture, Department of Anesthesiology, School of Stomatology, Fourth Military Medical University, Xi'an, China.
Ceng LuoDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Yazhou WangDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-7116-2395
Shengxi WuDepartment of Neurobiology and Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-3210-9567
Air Force Medical University · CNYanan University Affiliated Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Social dysfunction is the core syndrome of autism spectrum disorder (ASD) and lacks effective medicine. Although numerous risk genes and relevant environmental factors have been identified, the convergent molecular mechanism underlying ASD-associated social dysfunction remains largely elusive. Here, we report aberrant activation of canonical Wnt signaling and increased glycolysis in the anterior cingulate cortex (ACC, a key brain region of social function) of two ASD mouse models (Shank3

Indexed as

Autism Spectrum DisorderAnimalsAxin ProteinDisease Models, AnimalGlycolysisHeterocyclic Compounds, 3-RingHumansMiceMicrofilament ProteinsNerve Tissue ProteinsNeuronsWnt Signaling PathwayAxin2 protein, mouseAxin ProteinHeterocyclic Compounds, 3-RingMicrofilament ProteinsNerve Tissue ProteinsShank3 protein, mouseXAV939Axin2glycolysissocial dysfunctionWnt signaling

Identifiers

PMID37078424
PMCPMC10245038
OpenAlexW4366462920

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.