Evidence map›Paper›PMID 42129177›Full record

ArticleNature communications2026

MeCP2 Governs maternal hyperandrogenism-induced cortical defects and behavioral alterations via noncanonical AR-dependent regulation of Mef2c.

Yu-Meng Wang, Yanyan Jia, Yu Wu, Qiaohang Zhao, Yumeng Guo, Li Zhang, Min Jin, Yufang Zheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

8 authors.

Yu-Meng Wang *Department of Cardiology, Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. yumeng1229@126.com.
Yanyan Jia *ENT Institute and Otorhinolaryngology Department of Eye & ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.ORCID 0000-0001-7089-0959
Yu Wu *Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Qiaohang ZhaoDepartment of Reproductive Medicine, the Second Affiliated Hospital, Medical School, Zhejiang University, Hangzhou, Zhejiang, China.
Yumeng GuoDepartment of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, China.
Li ZhangDepartment of Cardiology, Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. li.zhang@shsmu.edu.cn.ORCID 0000-0002-6906-3275
Min JinDepartment of Reproductive Medicine, the Second Affiliated Hospital, Medical School, Zhejiang University, Hangzhou, Zhejiang, China. min_jin@zju.edu.cn.ORCID 0000-0002-1390-4549
Yufang ZhengObstetrics and Gynecology Hospital, The institute of Obstetrics and Gynecology, Shanghai key lab of reproduction and development, Shanghai key lab of female reproductive endocrine related diseases, Fudan University, Shanghai, China. zhengyf@fudan.edu.cn.ORCID 0000-0002-0488-2624

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81901159
6 · The paper itself

Abstract

Elevated prenatal androgen levels have been associated with an increased incidence of several neurodevelopmental conditions in offspring. However, the underlying mechanisms remain poorly understood. Here we showed that elevated prenatal androgens, modeled via aromatase inhibition in mice, disrupt cortical development and behavior in male offspring by activating androgen receptors (AR). AR interacts with MeCP2 to upregulate the transcription factor MEF2C, bypassing standard androgen response elements. Knocking down Mecp2 or Mef2c, or blocking AR, reversed these effects. Mecp2 duplication alone also upregulated MEF2C, driving similar neurogenesis and behavioral changes that were reversed by AR blockade. This reveals a MeCP2-mediated, non-canonical pathway by which androgens may contribute to male-biased neurodevelopmental conditions.

Indexed as

AndrogensCerebral CortexMEF2 Transcription FactorsMethyl-CpG-Binding Protein 2Prenatal Exposure Delayed EffectsReceptors, AndrogenAnimalsBehavior, AnimalFemaleMaleMiceNeurogenesisPregnancyAndrogensAR protein, mouseMecp2 protein, mouseMef2c protein, mouseMEF2 Transcription FactorsMethyl-CpG-Binding Protein 2Receptors, Androgen

Identifiers

PMID42129177
PMCPMC13171901

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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.