Evidence map›Paper›PMID 39002004›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2024

Effect of α7 nAChR-autophagy axis of deciduous tooth pulp stem cells in regulating IL-1β in the process of physiological root resorption of deciduous teeth.

Tiankai Di, Yujiang Chen, Zhifei Zhou, Jiajia Liu, Yang Du, Chao Feng, Bin Zhu, Lulu Wang

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

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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.

Tiankai Di *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Yujiang Chen *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Zhifei ZhouDepartment of Stomatology, General Hospital of Tibet Military Region, Lhasa, 850007, People's Republic of China.
Jiajia LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Yang DuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China.
Chao FengDepartment of Stomatology, The 969th Hospital, Joint Logistics Support Force of the Chinese People's Liberation Army, Hohhot, Inner Mongolia, 010000, People's Republic of China.
Bin ZhuDepartment of Stomatology, General Hospital of Tibet Military Region, Lhasa, 850007, People's Republic of China. antony-2004@163.com.
Lulu WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, People's Republic of China. wanglulufmmu@hotmail.com.ORCID 0000-0001-8789-3400

Funding

Key Research and Development Projects of Shaanxi Province 2022KW-12National Natural Science Foundation of China 81800924National Natural Science Foundation of China 82100954Natural Science Basic Research Program of Shaanxi Province 2022JQ-915Natural Science Basic Research Program of Shaanxi Province 2024JC-YBMS-687Natural Science Foundation of Inner Mongolia Autonomous Region 2023QN08026
6 · The paper itself

Abstract

Physiological root resorption of deciduous teeth is a normal phenomenon occurring during the developmental stages of children. Previous research has indicated the pivotal role of the inflammatory microenvironment in this process, although the specific mechanisms remain unclear. This study is aimed at elucidating the involvement of the alpha7 nicotinic acetylcholine receptors (α7 nAChR)-autophagy axis in the regulation of the inflammatory microenvironment during physiological root resorption in deciduous teeth. Samples were collected from deciduous teeth at various stages of physiological root resorption, and deciduous dental pulp stem cells (DDPSCs) were isolated and cultured during the mid-phase of root resorption. The findings revealed a substantial infiltration of the pulp of deciduous teeth at the mid-phase of root resorption, characterized by elevated expression levels of α7 nAChR and IL-1β. Significantly increased IL-1β and α7 nAChR expressions were observed in DDPSCs during the mid-phase of root resorption, with α7 nAChR demonstrating a regulatory effect on IL-1β. Moreover, evidence suggested that mechanical stress may act as a trigger, regulating autophagy and IL-1 expression via α7 nAChR. In conclusion, mechanical stress was identified as a regulator of autophagy in DDPSCs through α7 nAChR, influencing the expression of IL-1β and contributing to the formation of the inflammatory microenvironment. This mechanism plays a crucial role in the physiological root resorption of deciduous teeth. KEY MESSAGES: The pulp of deciduous teeth at mid-phase of root resorption was heavily infiltrated with high expression of α7nAChR and IL-1β. α7 nAChR acts as an initiating factor to regulate IL-1β through autophagy in DDPSCs. Mechanical stress can regulate autophagy of DDPSCs through α7 nAChR and thus affect IL-1β expression and inflammatory microenvironment formation in physiological root resorption in deciduous teeth.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAutophagyDental PulpInterleukin-1betaRoot ResorptionStem CellsTooth, DeciduousCells, CulturedChildHumansalpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, humanIL1B protein, humanInterleukin-1betaAutophagyDeciduous dental pulp stem cellsIL-1βMechanical stressPhysiological root resorptionα7 nAChR

Identifiers

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Read underepoch 390

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.