Evidence map›Paper›PMID 41948101›Full record

ArticleInternational journal of genomics2026

A Cross-Tissue Multiomics Analysis Reveals the Protective Role of TGFBR3 in Postmenopausal Osteoporosis.

Yimin Liu, Chenxu Xie, Kaiwen Yang, Zixuan Liu, Runtong Liu, Xiaoli Hou, Lei Xing, Jingyuan Gao, Qiangqiang Lian, Yunpeng Hu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Yimin LiuClinical Medical College, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.ORCID https://orcid.org/0009-0000-9877-2129
Chenxu XieClinical Medical College, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Kaiwen YangClinical Medical College, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Zixuan LiuSchool of Public Health, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Runtong LiuSchool of Public Health, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Xiaoli HouSchool of Public Health, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Lei XingDepartment of Geriatrics, Affiliated Hospital of North China University of Science and Technology, Tangshan, 063099, Hebei, China.
Jingyuan GaoDepartment of Geriatrics, Affiliated Hospital of North China University of Science and Technology, Tangshan, 063099, Hebei, China.
Qiangqiang LianSchool of Public Health, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Yunpeng HuDepartment of Orthopedic Surgery, The Second Hospital of Tangshan, Tangshan, 063000, Hebei, China.
Yongheng WangSchool of Public Health, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Liu ZhangSchool of Public Health, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.
Faming TianClinical Medical College, North China University of Science and Technology, Tangshan, 063210, Hebei, China, ncst.edu.cn.ORCID https://orcid.org/0000-0001-7083-3380

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Postmenopausal osteoporosis (PMO) develops as a result of pathological cross-tissue interactions. However, current experimental paradigms are constrained by their single-tissue focus, hindering efforts to discover systemwide regulatory genes. Objective: We aimed to discover conserved genetic regulators of PMO by integrating cross-tissue transcriptomic profiles in humans and to characterize their biological functions via combined genetic epidemiology and experimental studies using integrated analytical strategies. Methods: Our analytical framework encompassed transcriptome profiles from human peripheral blood mononuclear cells, bone marrow, and bone tissue. We adopted a tiered strategy involving differential expression analysis, weighted gene coexpression network construction, and machine learning with 108 algorithm combinations for candidate gene selection. A two-sample Mendelian randomization was used to inform causal gene-disease relationships, while the key results were validated in an ovariectomized mouse model of osteoporosis. Mechanistic studies included single-cell transcriptomics, functional enrichment, and immune microenvironment profiling. Results: Cross-tissue analysis identified 97 consistently dysregulated genes between tissues, which were further refined to 64 high-confidence candidates. TGFBR3 was significantly protective against PMO (IVW OR = 0.675, 95% CI: 0.466-0.977, Conclusion: This is the first study to identify TGFBR3 as a novel cross-tissue protective regulator of PMO. Our integrated approach covering genomic discovery, causal inference, and experimental validation offers strong support to the hypothesis that TGFBR3 deficiency constitutes a fundamental feature of PMO pathogenesis, while shedding light on its multilevel protective mechanisms.

Indexed as

machine learningMendelian randomizationpostmenopausal osteoporosissingle-cell transcriptomicsTGFBR3

Identifiers

PMID41948101
PMCPMC13051796

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.