Evidence map›Paper›PMID 41385921›Full record

ArticleInternational dental journal2026

Mechanosensitive Yes-Associated Protein/TAZ-cGAS-STING Axis Induces Periodontal Ligament Fibroblasts Senescence and Mediates Compression-Induced Root Resorption.

Zuping Wu, Siqi Bao, Qian Chen, Xiao Lu, Guzhe Guan, Ruifeng Song, Qianming Chen, Xiaoyan Chen

Erratum issuedAbstract read
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In one paragraph

Article in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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

5 · Who and what money

Authors and funding

8 authors.

Zuping WuStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China; Guangxi Key Laboratory of the Rehabilitation and Reconstruction for Oral and Maxillofacial Research, Affiliated Hospital of Stomatology, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.
Siqi BaoStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China.
Qian ChenStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China.
Xiao LuCase Western Reserve University Dental School, Cleveland, Ohio, USA.
Guzhe GuanStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China.
Ruifeng SongStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China.
Qianming ChenStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China. Electronic address: qmchen@zju.edu.cn.
Xiaoyan ChenStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China. Electronic address: ortho_chenxy@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study investigates compressive force-induced senescence in periodontal ligament fibroblasts (PDLFs) and its mechanistic role in orthodontic root resorption. MATERIALS AND

methodsPDLFs senescence under compressive forces was evaluated using β-galactosidase staining, Western blotting, and immunofluorescence. Functional consequences of senescence were assessed via Alizarin Red S for mineralization and TRAP staining for osteoclast differentiation. Yes-associated protein (YAP) signalling dynamics were analysed through Western blot and immunofluorescence, with pharmacological activation by XMU-MP-1. The interplay between YAP and the cGAS/STING pathway was investigated using pharmacological interventions. Finally, senescence-mediated effects on mineralization and osteoclastogenesis were evaluated post-treatment with pathway-specific agonists or inhibitors.

resultsCompressive forces induced senescence in PDLFs, evidenced by SA-β-gal activation and reduced mineralization capacity. Coculture with osteoclast precursors amplified osteoclast differentiation. Mechanistically, compressive forces inactivated mechanosensitive YAP, triggering senescence, rescued by YAP agonist XMU-MP-1. The YAP/cGAS/STING axis was identified as central: YAP inactivation upregulated cGAS/STING signalling, while STING agonist c-di-GMP exacerbated senescence and impaired mineralization. Pharmacological validation confirmed bidirectional regulation - YAP activation reduced senescence/osteoclastogenesis, whereas STING inhibition reversed these effects.

conclusionMechanical stress-induced YAP dysfunction drives PDLF senescence via cGAS/STING pathway activation, establishing a novel mechanobiological axis in root resorption.

Indexed as

Adaptor Proteins, Signal TransducingCellular SenescenceFibroblastsMembrane ProteinsNucleotidyltransferasesPeriodontal LigamentRoot ResorptionTranscription FactorsCell DifferentiationCells, CulturedHumansMechanotransduction, CellularOsteoclastsOsteogenesisSignal TransductionSTING ProteinAdaptor Proteins, Signal TransducingMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinscGAS/STINGPeriodontal ligament fibroblastsRoot resorptionSenescenceYAP

Identifiers

PMID41385921
PMCPMC12757478

What Socratic 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 Socratic graph.