Evidence map›Paper›PMID 42156771›Full record

ArticleNature communications2026

TGFβ-mediated dural progenitor cell migration into the coronal suture is crucial for preventing craniosynostosis.

Peng Chen, Lin Meng, Lin Lan, Jifan Feng, Tingwei Guo, Lu Gao, Hana Hekmat, Calista Ly, Mingyi Zhang, Sa Cha and 2 more

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. 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

12 authors.

Peng Chen *Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Lin Meng *Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-2162-4678
Lin LanCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Jifan FengCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Tingwei GuoCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Lu GaoCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Hana HekmatCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Calista LyCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Mingyi ZhangCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Sa ChaCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0003-4126-8620
Thach-Vu HoCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
Yang ChaiCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA. ychai@usc.edu.ORCID http://orcid.org/0000-0003-2477-7247

Funding

Mechanisms and rescue of craniosynostosis associated with gene-environment interactionR01DE030901 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAI, YANG, CHEN, JIANFU · 2021 to 2025
$3.0M
NIDCR NIH HHS R01 DE030901U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) R01DE0030901
6 · The paper itself

Abstract

Cranial sutures are essential for skull growth and tissue homeostasis. Among them, the coronal suture is most frequently affected in syndromic craniosynostosis, yet the mechanisms underlying this preferential involvement remain unclear. Here, we show that the coronal suture mesenchyme undergoes a postnatal lineage transition from mesodermal to cranial neural crest origin, facilitated by dural cell migration into the suture. Mechanistically, this migration is regulated by suture TGFβ signals to Tgfbr2+ dural cells. Loss of dural Tgfbr2 impairs this cell migration into the suture, reduces the Gli1+ suture progenitor pool, and causes premature coronal suture fusion. Furthermore, in Twist1

Indexed as

Cell MovementCranial SuturesCraniosynostosesDura MaterStem CellsTransforming Growth Factor betaAcrocephalosyndactyliaAnimalsHumansMesodermMiceMice, KnockoutNeural CrestNuclear ProteinsReceptor, Transforming Growth Factor-beta Type IISignal TransductionGli1 protein, mouseNuclear ProteinsReceptor, Transforming Growth Factor-beta Type IITgfbr2 protein, mouseTransforming Growth Factor betaTwist1 protein, mouseTwist-Related Protein 1Zinc Finger Protein GLI1

Identifiers

PMID42156771
PMCPMC13381870

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.