Evidence map›Paper›PMID 42414968›Full record

ArticleBMC oral health2026

Regulatory effects of transcription factor PAX3 on human dental pulp stem cells.

Zengguo Chen, Huijuan Liu, Xue Zhang, Dandan Li, Wenjing Li

Abstract read
In one paragraph

Article in BMC oral health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Zengguo ChenDepartment of Oral Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Huijuan LiuHebei Key Laboratory of Stomatology, Hebei Technology Innovation Center of Oral Health, School and Hospital of Stomatology, Hebei Medical University, Shijiazhuang, 050017, China.
Xue ZhangDepartment of Oral Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Dandan LiDepartment of Cariology and Endodontics, Jinan Stomatological Hospital, Jinan, 250001, China.
Wenjing LiDepartment of Oral Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China. 27801072@hebmu.edu.cn.ORCID https://orcid.org/0009-0005-7490-7507

Funding

Hebei Provincial Government-Funded Clinical Medical Outstanding Talents Project 303-2022-27-41
6 · The paper itself

Abstract

backgroundDental pulp stem cells (DPSCs) are promising for regenerative dentistry but undergo replicative senescence during in vitro expansion, leading to diminished proliferative capacity and osteogenic potential. This study aimed to investigate the role of the transcription factor PAX3 in regulating the senescence process of human DPSCs (hDPSCs).

methodsA replicative senescence model of hDPSCs was established through serial passaging (P3 as young cells vs. P11 as senescent cells). The expression of PAX3 and senescence markers (p53, p21) was assessed. The functional role of PAX3 was investigated by knocking it down (si-PAX3) or overexpressing it (OE-PAX3) in hDPSCs, followed by evaluations of senescence-associated β-galactosidase (SA-β-gal) activity, cell proliferation, and osteogenic differentiation.

resultsPAX3 expression was significantly downregulated in senescent P11 hDPSCs compared to young P3 cells. Functionally, PAX3 knockdown was associated with accelerated cellular senescence, as evidenced by increased SA-β-gal activity, upregulation of p53 and p21 mRNA levels, impaired cell proliferation, and reduced osteogenic differentiation. Conversely, PAX3 overexpression was associated with an attenuated senescent phenotype, resulting in decreased SA-β-gal activity and expression of p53/p21, enhanced proliferation, and improved osteogenic capacity.

conclusionThe transcription factor PAX3 may play a critical regulatory role in mitigating hDPSCs senescence, as downregulation of PAX3 was associated with increased senescence markers and its overexpression with reduced senescence markers. The observed correlation with p53/p21 mRNA levels suggests that this pathway may be involved, but mechanistic validation at the protein level is still required. These findings indicate that PAX3 represents a candidate for further investigation as a potential target to delay senescence and maintain the functional properties of hDPSCs, warranting further investigation for its potential utility in tissue engineering and clinical stem cell-based therapies.

Indexed as

Dental PulpPaired Box Transcription FactorsPAX3 Transcription FactorStem CellsCell DifferentiationCell ProliferationCells, CulturedCellular SenescenceHumansOsteogenesisTumor Suppressor Protein p53Paired Box Transcription FactorsPAX3 protein, humanPAX3 Transcription FactorTumor Suppressor Protein p53Dental pulp stem cellsOsteogenic differentiationPAX3ProliferationSenescence

Identifiers

PMID42414968
PMCPMC13628945

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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.