Evidence map›Paper›PMID 40395150›Full record

ArticleCNS neuroscience & therapeutics2025

Calcitriol Modulates Hippocampal Axon Guidance Through Enhanced EfnA4-Mediated PI3K/AKT Signaling in an Autism Mouse Model.

Tiantian Gong, Ruizhen Sun, Jieli Bai, Xin Liu, Chenyao He, Qi Jiang, Qi Wang, Yubo Qi, Wenxin Ding, Jingling Shen and 2 more

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
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

12 authors.

Tiantian GongDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.ORCID 0009-0002-4501-7191
Ruizhen SunDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Jieli BaiDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Xin LiuDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Chenyao HeDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Qi JiangGuangzhou Laboratory, Guangzhou International Bio Island, Guangzhou, China.
Qi WangDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Yubo QiDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Wenxin DingDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Jingling ShenInstitute of Life Sciences, College of Life and Environmental Science, Wenzhou University, Wenzhou, China.
Lei LeiDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Zhiyan ShanDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Funding

National Natural Science Foundation of China 82271888Natural Science Foundation of Heilongjiang Province LH2024H022
6 · The paper itself

Abstract

aimsAutism spectrum disorder (ASD) is a complex neurodevelopmental condition arising from the interplay of genetic predispositions and environmental influences. Recent studies have suggested that vitamin D (VitD) supplementation play a role in reducing the risk of ASD and alleviating some of its core symptoms. However, variations in individual responses to VitD due to biological heterogeneity have led to inconsistent clinical outcomes, and the precise molecular mechanisms through which VitD might exert its effects on ASD remain poorly understood.

methodsWe investigated the effects of calcitriol, the biologically active form of VitD, on ASD-associated phenotypes in BTBR mice, a well-established autism model. Behavioral assessments were used to evaluate social and repetitive behaviors. Mechanistic insights were obtained through RNA sequencing, immunohistochemistry, biochemical assays, and stripe guidance assays.

resultsCalcitriol supplementation significantly improved autism-like behaviors in BTBR mice, alleviating hippocampal hypoplasia and correcting axon guidance abnormalities. These effects were mediated by modulation of the EfnA4-PI3K signaling pathway in hippocampal neural progenitor cells and other brain regions, highlighting its role in neurodevelopmental processes.

conclusionOur findings demonstrate that calcitriol targets axon-guidance-related signaling pathways, providing a theoretical framework and potential clinical strategy for targeted ASD interventions.

Indexed as

Autistic DisorderAxon GuidanceCalcitriolHippocampusAnimalsAutism Spectrum DisorderDisease Models, AnimalMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCalcitriolPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktautism spectrum disorderaxon guidancebehaviorscalcitriolhippocampus

Identifiers

PMID40395150
PMCPMC12093051

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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.