Evidence mapPaperPMID 42392085Full record

ArticleStem cell reports2026

Neural stem cells as potential mediators of prenatal dietary stress through epigenetic mechanisms.

Itsuki Kageyama, Hiroya Yamada, Mirai Yamazaki, Takuya Wakasugi, Yuri Kamiya, Masaki Ohshiro, Manaka Ito, Yoshiki Tsuboi, Takashi Watanabe, Genki Mizuno and 5 more

Abstract read
In one paragraph

Article in Stem cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Itsuki KageyamaDepartment of Hygiene, Fujita Health University School of Medicine, Toyoake, Japan; Department of Preventive Medical Sciences, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Hiroya YamadaDepartment of Hygiene, Fujita Health University School of Medicine, Toyoake, Japan. Electronic address: hyamada@fujita-hu.ac.jp.
Mirai YamazakiDepartment of Hygiene, Fujita Health University School of Medicine, Toyoake, Japan.
Takuya WakasugiDepartment of Hygiene, Fujita Health University School of Medicine, Toyoake, Japan.
Yuri KamiyaDepartment of Hygiene, Fujita Health University School of Medicine, Toyoake, Japan.
Masaki OhshiroDepartment of Informative Clinical Medicine, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Manaka ItoDepartment of Informative Clinical Medicine, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Yoshiki TsuboiDepartment of Preventive Medical Sciences, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Takashi WatanabeDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.
Genki MizunoDepartment of Medical Technology, Tokyo University of Technology School of Health Sciences, Ota, Japan.
Yoshitaka AndoDepartment of Informative Clinical Medicine, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Hiroaki IshikawaDepartment of Informative Clinical Medicine, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Koji SuzukiDepartment of Preventive Medical Sciences, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Koji OhashiDepartment of Informative Clinical Medicine, Fujita Health University School of Medical Sciences, Toyoake, Japan.
Eiji MunetsunaDepartment of Hygiene, Fujita Health University School of Medicine, Toyoake, Japan; Department of Animal Science and Biotechnology, Azabu University School of Veterinary Medicine, Sagamihara, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The developmental origins of health and disease (DOHaD) hypothesis suggests that environmental exposures during development can induce long-term health effects, yet the cellular origin of such persistence remains unclear. Here, we suggest that neural stem cells (NSCs) may develop aberrant properties that persist with possible involvement of epigenetic mechanisms linking maternal dietary stress to neurocognitive impairments. In a rat model of maternal high-fructose corn syrup intake, offspring showed hippocampus-dependent memory deficits and reduced neurogenesis. NSCs from fetal and adolescent hippocampi exhibited persistent dysfunction with transcriptomic dysregulation. Mechanistically, transient downregulation of DNA methyltransferase 3A in fetal NSCs was associated with sustained repression of secreted phosphoprotein 1, encoding intracellular osteopontin (iOPN). iOPN overexpression partially restored NSC function, supporting a potential causal link. Our study proposes a DOHaD framework in which stem cells with lasting alterations may retain epigenetic traces of early life stress, with implications for organ systems and disease risk.

Indexed as

DietEpigenesis, GeneticNeural Stem CellsPrenatal Exposure Delayed EffectsStress, PhysiologicalAnimalsDevelopmental Origins of Health and DiseaseDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3AFemaleFructoseHippocampusNeurogenesisOsteopontinPregnancyDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AFructoseOsteopontinDNA methylationDOHaDepigeneticsfructoseosteopontinstem cell programming

Identifiers

PMID42392085
PMCPMC13385421

What Socratic 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 Socratic graph.