Evidence map›Paper›PMID 39556706›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Deficiency of FABP7 Triggers Premature Neural Differentiation in Idiopathic Normocephalic Autism Organoids.

Xiao Han, Yuanlin He, Yuanhao Wang, Wenzhu Hu, Chu Chu, Lei Huang, Yuan Hong, Lu Han, Xu Zhang, Yao Gao and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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  4. FABP7 controls radial glial scaffold stability during human cortical development.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

16 authors.

Xiao HanInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.
Yuanlin HeInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.
Yuanhao WangInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.
Wenzhu HuDepartment of Epidemiology and Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Chu ChuInstitute of Stem Cell and Neural Regeneration, School of Pharmacy, Nanjing Medical University, Nanjing, 211166, China.
Lei HuangInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.
Yuan HongInstitute of Stem Cell and Neural Regeneration, School of Pharmacy, Nanjing Medical University, Nanjing, 211166, China.
Lu HanAutism Research Center, State Key Laboratory of Reproductive Medicine, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, 210029, China.
Xu ZhangInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.
Yao GaoDepartment of Epidemiology and Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Yuan LinInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.
Hongxia MaInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.
Hongbing ShenDepartment of Epidemiology and Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Xiaoyan KeAutism Research Center, State Key Laboratory of Reproductive Medicine, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, 210029, China.
Yan LiuInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.ORCID 0000-0003-2918-5398
Zhibin HuInterdisciplinary Inno Center for Organoids, State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, 211166, China.

Funding

National Key Research and Development Program of China 2019YFA0802703National Key Research and Development Program of China 2021YFA1101800National Key Research and Development Program of China 2021YFC2700600National Natural Science Foundation of China 52033002National Natural Science Foundation of China 82171528National Natural Science Foundation of China 82325015
6 · The paper itself

Abstract

Autism spectrum disorder (ASD), which is caused by heterogeneous genetic and environmental factors, is characterized by diverse clinical phenotypes linked to distinct pathological mechanisms. ASD individuals with a shared clinical phenotype might contribute to revealing the molecular mechanism underlying ASD progression. Here, it is generated induced pluripotent stem cell (iPSC)-derived cerebral organoids from normocephalic individuals with ASD in a prospective birth cohort with a shared clinical diagnosis. Multiple cell lines and time series scRNA-seq combined with a histomorphological analysis revealed premature neural differentiation of neural stem cells (NSCs) and decreased expression of Fatty acid binding protein 7 (FABP7) in ASD organoids. It is subsequently revealed alterations in the phosphorylation levels of Mitogen-Activated Protein Kinase Kinase 1/2 (MEK1/2), which are downstream of FABP7, and the regulation of the FABP7/MEK pathway reversed improper neural differentiation in the ASD organoids. Moreover, both Fabp7-knockdown and MEK2-overexpressing mice exhibited repetitive stereotyped behaviors and social defects relevant to autism. This study reveals the role of the FABP7/MEK pathway in abnormal NSC differentiation in normocephalic individuals with ASD, which might provide a promising therapeutic target for ASD treatment.

Indexed as

Autism Spectrum DisorderAutistic DisorderCell DifferentiationFatty Acid-Binding Protein 7Neural Stem CellsOrganoidsAnimalsFemaleHumansInduced Pluripotent Stem CellsMaleMiceTumor Suppressor ProteinsFABP7 protein, humanFatty Acid-Binding Protein 7Tumor Suppressor Proteinsautism spectrum disordercerebral organoidFABP7normocephalypremature neural differentiation

Identifiers

PMID39556706
PMCPMC11727249

What OpenQuestion holds

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Registered trials

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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.