Evidence map›Paper›PMID 41268237›Full record

ArticleAmerican journal of translational research2025

Transcriptome analysis of induced pluripotent stem cells' osteogenic differentiation reveals NPY1R activating PI3K/AKT/mTOR in alveolar bone loss during periodontitis.

Xiaowen Li, Ruikang Guo, Lingling Liang, Hao Liang, Guangqi Zhou, Qinglan Lu, Yonghui Huang, Zhen Qi, Xiaojie Li

Abstract read
PubMed Full text at PMC Publisher
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Article in American journal of translational research, 2025. 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

What it found

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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

The trial behind it

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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

9 authors.

Xiaowen LiGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, College and Hospital of Stomatology, Guangxi Medical University Nanning 530021, Guangxi, P. R. China.
Ruikang GuoDepartment of Cardiovascular Surgery, The Second Xiangya Hospital, Central South University Changsha 410000, Hunan, P. R. China.
Lingling LiangGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, College and Hospital of Stomatology, Guangxi Medical University Nanning 530021, Guangxi, P. R. China.
Hao LiangGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, College and Hospital of Stomatology, Guangxi Medical University Nanning 530021, Guangxi, P. R. China.
Guangqi ZhouGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, College and Hospital of Stomatology, Guangxi Medical University Nanning 530021, Guangxi, P. R. China.
Qinglan LuGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, College and Hospital of Stomatology, Guangxi Medical University Nanning 530021, Guangxi, P. R. China.
Yonghui HuangGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, College and Hospital of Stomatology, Guangxi Medical University Nanning 530021, Guangxi, P. R. China.
Zhen QiDepartment of Cardiovascular Surgery, The Second Xiangya Hospital, Central South University Changsha 410000, Hunan, P. R. China.
Xiaojie LiGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, College and Hospital of Stomatology, Guangxi Medical University Nanning 530021, Guangxi, P. R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePeriodontitis, a prevalent oral disease leading to alveolar bone defects, remains a primary cause of tooth loss in adults. The biologic mechanisms driving bone loss in periodontitis are still poorly understood, limiting the development of genetic treatment. This study investigates potential therapeutic targets for alveolar bone loss by analyzing transcriptomic data related to the osteogenic differentiation of induced pluripotent stem cells (iPSCs).

methodsUsing

resultsTranscriptomic profiling during iPSC osteogenic differentiation revealed significant upregulation of neuropeptide Y (NPY) and NPY1R. Suppression of NPY1R reduced the osteogenic capacity of iPSCs. Activation of the PAM pathway was observed during osteogenesis, and treatment with LY294002, a PAM pathway inhibitor, led to decreased osteogenic activity.

conclusionThe NPY/NPY1R axis and the PAM signaling pathway appear to regulate bone regeneration and may be involved in preventing alveolar bone loss in periodontitis. These findings provide a new direction for therapy targeting bone defects associated with periodontal disease.

Indexed as

bioinformatics analysisiPS cellNPY1RperiodontitisPI3K/mTOR pathwaytherapeutic target

Identifiers

PMID41268237
PMCPMC12628227

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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.