Evidence map›Paper›PMID 33542209›Full record

ArticleCell death & disease2021

Osteomodulin positively regulates osteogenesis through interaction with BMP2.

Wenzhen Lin, Xiaohan Zhu, Li Gao, Mengying Mao, Daming Gao, Zhengwei Huang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.4field-weighted citation impact, top 4% of its field
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

39 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  3. Bone matrix proteins: regulators of skeletal remodeling and repair.Journal of bone and mineral metabolism · 2026
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  18. Osteomodulin deficiency in mice causes a specific reduction of transversal cortical bone size.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
    Article
  19. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Wenzhen Lin *Department of Endodontics, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaohan Zhu *Department of Endodontics, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Li GaoDepartment of Endodontics, Shanghai Stomatological Hospital, Fudan University, Shanghai, China.
Mengying MaoDepartment of Endodontics, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Daming GaoState Key Laboratory of Cell Biology, CAS Key Laboratory of Systems Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0003-4374-1055
Zhengwei HuangDepartment of Endodontics, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. huangzhengwei@shsmu.edu.cn.ORCID 0000-0001-9861-514X
Shanghai Jiao Tong University · CNChinese Academy of Sciences · CNFudan University · CNNational Clinical Research Center for Digestive Diseases · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteomodulin (OMD), a member of the small leucine-rich proteoglycan family, distributes in mineralized tissues and is positively regulated by bone morphogenetic protein 2 (BMP2). However, the exact function of OMD during mineralization and its association with BMP2 remain poorly understood. Herein, the expression pattern of OMD during osteogenesis was investigated in human dental pulp stem cells. Silencing OMD gene significantly suppressed the alkaline phosphatase activity, mineralized nodule formation and osteogenesis-associated gene transcription. Besides, OMD could enhance BMP2-induced expression of SP7 and RUNX2 with concentration dependence in vitro. Rat mandibular bone defect model revealed that scaffolds injected with the combination of OMD and suboptimal BMP2 exhibited more mature and abundant mineralized bone than that treated with OMD or suboptimal BMP2 alone. Mechanistically, OMD could bind to BMP2 via its terminal leucine-rich repeats and formed complexes with BMP2 and its membrane receptors, thus promoting BMP/SMAD signal transduction. In addition, OMD was a putative target gene of SMAD4, which plays a pivotal role in this pathway. Collectively, these data elucidate that OMD may act as a positive coordinator in osteogenesis through BMP2/SMADs signaling.

Indexed as

AnimalsBone Morphogenetic Protein 2Cell DifferentiationExtracellular Matrix ProteinsHumansOsteogenesisProteoglycansRatsTranscription FactorsBMP2 protein, humanBone Morphogenetic Protein 2Extracellular Matrix ProteinsosteoadherinProteoglycansTranscription Factors

Identifiers

PMID33542209
PMCPMC7862363
OpenAlexW3126912938

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.