Evidence map›Paper›PMID 41309624›Full record

ArticleNature communications2025

Autocrine ECM molecules establish MSC quiescence during incisor development by disrupting WNT ligand trafficking process.

Zexi Chen, Meilian Cai, Yuling Wang, Xuan Li, Yongwen He, Hongji Pu, Juan Huang, Ling Ye, Ruili Yang, Junjun Jing and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2025. 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

11 authors.

Zexi Chen *Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.
Meilian Cai *Chinese Institute for Brain Research, Beijing, China.
Yuling WangChinese Institute for Brain Research, Beijing, China.
Xuan LiState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Yongwen HeQujing Medical College, Qujing City, Yunnan Province, China.
Hongji PuQujing Medical College, Qujing City, Yunnan Province, China.
Juan HuangChinese Institute for Brain Research, Beijing, China.
Ling YeState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.ORCID http://orcid.org/0000-0002-8417-7676
Ruili YangDepartment of Orthodontics, Peking University School and Hospital of Stomatology, National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China. ruiliyang@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-3283-9893
Junjun JingState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. junjunjing@scu.edu.cn.ORCID http://orcid.org/0009-0002-8608-8316
Hu ZhaoChinese Institute for Brain Research, Beijing, China. zhaohu@cibr.ac.cn.ORCID http://orcid.org/0000-0002-2961-0086

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stem cells support homeostasis and injury repair of adult organs. It remains unclear when and how adult stem cells form during development. Here, we discover that incisor mesenchymal stem cells, marked by an extracellular matrix molecule Smoc2, establish their identity and quiescence between E14.5 and E16.5, and persist into adulthood. They support both embryonic tooth development and postnatal organ turnover. Concurrently, the incisor mesenchyme evolves from a homogenous dental papilla into a heterogeneous dental pulp consisting of a complete lineage hierarchy, which persists into adulthood. Smoc2 and its homologous molecule Smoc1 are indispensable for maintaining the quiescence and hierarchy of mesenchymal stem cells. They function by disrupting the binding between canonical WNT ligands and glypican, a process critical for transporting hydrophobic WNT ligands within the aqueous niche. In conclusion, mesenchymal stem cells establish their quiescence during development through autocrine extracellular matrix molecules to keep canonical WNT ligands from accessing them.

Indexed as

Autocrine CommunicationExtracellular MatrixIncisorMesenchymal Stem CellsWnt ProteinsAnimalsDental PapillaDental PulpFemaleGlypicansLigandsMaleMiceOdontogenesisReceptors, G-Protein-CoupledWnt Signaling PathwayGlypicansGpr177 protein, mouseLigandsReceptors, G-Protein-CoupledWnt Proteins

Identifiers

PMID41309624
PMCPMC12660891

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.