Evidence map›Paper›PMID 41326797›Full record

ArticleCommunications biology2025

Integrative analysis reveals synergistic regulation of Sp7 by BRD9 and Wnt/β-catenin signaling during osteogenic differentiation.

Longfei Wu, Lei Wang, Yan Zhuang, Yuan Luo, Qingyun Zhu, Muyesaier Maimaitizunong, Yanfei Wang, Zijian Cheng, Yulong Li, Xinrui Sheng and 7 more

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

17 authors.

Longfei Wu *Center for Genetic Epidemiology and Genomics, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China. lfwu@suda.edu.cn.ORCID http://orcid.org/0000-0003-3594-3853
Lei Wang *Center for Genetic Epidemiology and Genomics, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China.
Yan Zhuang *Taicang Affiliated Hospital, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, China.
Yuan Luo *Taicang Affiliated Hospital of Soochow University, Suzhou, China.
Qingyun ZhuCenter for Genetic Epidemiology and Genomics, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China.
Muyesaier MaimaitizunongTaicang Affiliated Hospital, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, China.
Yanfei WangCenter for Genetic Epidemiology and Genomics, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China.
Zijian ChengCenter for Genetic Epidemiology and Genomics, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China.ORCID http://orcid.org/0009-0004-6421-0389
Yulong LiSchool of Life Sciences, Inner Mongolia University, Hohhot, China.
Xinrui ShengCenter for Genetic Epidemiology and Genomics, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China.
Mengjie LiCambridge-Suda Genomic Resource Center, Suzhou Medical College of Soochow University, Suzhou, China.
Qi'an LuoCambridge-Suda Genomic Resource Center, Suzhou Medical College of Soochow University, Suzhou, China.
Xiyuan JiangCenter of Osteoporosis, Kunshan Hospital of Traditional Chinese Medicine, Suzhou, China.
Shufeng LeiCenter for Genetic Epidemiology and Genomics, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China.
Xinhua LinCambridge-Suda Genomic Resource Center, Suzhou Medical College of Soochow University, Suzhou, China.
Yingbin ZhongTaicang Affiliated Hospital, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, China. ybzhongsd@suda.edu.cn.ORCID http://orcid.org/0000-0001-5896-6578
Wenyan RenCambridge-Suda Genomic Resource Center, Suzhou Medical College of Soochow University, Suzhou, China. rwy@suda.edu.cn.ORCID http://orcid.org/0000-0001-5794-8757

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31701273National Natural Science Foundation of China (National Science Foundation of China) 31871186National Natural Science Foundation of China (National Science Foundation of China) 82471841
6 · The paper itself

Abstract

Osteoporosis is a complex skeletal disorder characterized by low bone mineral density (BMD). Compared with classical epigenetic modifications, such as DNA methylation and histone modifications, the participation of chromatin-remodeling complexes in osteoporosis remains less explored. To identify chromatin remodeling factors causally associated with bone mineral density (BMD), here we conducted a systematic analysis of 87 genes encoding components of four major chromatin-remodeling complexes using Summary-data-based Mendelian randomization (SMR) analysis. Candidate chromatin-remodeling factors were further cross-referenced with publicly available skeletal phenotyping data from the International Mouse Phenotyping Consortium (IMPC) database. Functional validation revealed that non-canonical BAF (ncBAF) subunit BRD9 is essential for osteoblast differentiation using both in vitro cell culture and in vivo zebrafish models. RNA-Sequencing (RNA-Seq) demonstrated that BRD9 orchestrates osteogenic differentiation by modulating Wnt/β-catenin signaling activity. Mechanistically, the osteogenic master transcription factor Sp7 was identified as a direct transcriptional target of BRD9, whose expression is coordinately controlled through the synergistic interplay between BRD9 and Wnt/β-catenin signaling during osteogenesis. Collectively, this study established a comprehensive framework for identifying causal genes implicated in osteoporosis and elucidated the previously unrecognized regulatory role of BRD9 in osteogenesis.

Indexed as

Cell DifferentiationDNA-Binding ProteinsOsteogenesisSp7 Transcription FactorTranscription FactorsWnt Signaling PathwayAnimalsBromodomain Containing ProteinsHumansMiceOsteoblastsOsteoporosisZebrafishBRD9 protein, humanBromodomain Containing ProteinsDNA-Binding ProteinsSp7 protein, mouseSp7 Transcription FactorTranscription Factors

Identifiers

PMID41326797
PMCPMC12775129

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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.