Evidence map›Paper›PMID 38987555›Full record

ReviewBone research2024

Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and disease.

Lifang Hu, Wei Chen, Airong Qian, Yi-Ping Li

Abstract readReview
In one paragraph

Review in Bone research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
214citing papers in PubMed, 3 pooled it
–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

214 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Protective role of irisin on bone in osteoporosis: a systematic review of rodent studies.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
    Pooled it
  4. Trial
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  6. Gut microbes · 2026
    Article
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  19. Artificial intelligence virtual bone organoids (AIVBOs).Journal of orthopaedic translation · 2026
    Review
  20. Article

154 more citing papers are in PubMed but not listed here.

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

4 authors.

Lifang HuLaboratory for Bone Metabolism, Xi'an Key Laboratory of Special Medicine and Health Engineering, Key Laboratory for Space Biosciences and Biotechnology, Research Center for Special Medicine and Health Systems Engineering, School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi, 710072, China.ORCID http://orcid.org/0000-0003-1648-4428
Wei ChenDivision in Cellular and Molecular Medicine, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, Tulane University, New Orleans, LA, 70112, USA.
Airong QianLaboratory for Bone Metabolism, Xi'an Key Laboratory of Special Medicine and Health Engineering, Key Laboratory for Space Biosciences and Biotechnology, Research Center for Special Medicine and Health Systems Engineering, School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi, 710072, China. qianair@nwpu.edu.cn.ORCID http://orcid.org/0000-0002-0740-9218
Yi-Ping LiDivision in Cellular and Molecular Medicine, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, Tulane University, New Orleans, LA, 70112, USA. yli81@tulane.edu.ORCID http://orcid.org/0000-0003-2188-6958

Funding

Inhibiting Periodontitis by Targeting Cathepsin K and Attenuating TLR SignalingR01DE023813 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2014 to 2023
$3.9M
Mechanistic basis of the role of Cbx3 in negatively regulating osteoclast differentiation through epigenetic modificationR01AR075735 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2019 to 2024
$2.4M
Cbfβ mediates articular cartilage regeneration and repair in agingR01AG056438 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2019 to 2023
$2.1M
Gα13 signaling attenuates periodontal inflammation and alveolar bone loss in the mouse model of age-associated periodontitisR01DE028264 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2018 to 2022
$1.8M
Characterizing the negative signaling in dendritic cells and macrophages to attenuate inflammation and bone destruction in Rheumatoid arthritisR01AR074954 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2020 to 2024
$1.6M
Characterizing the mechanism by which endogenous negative regulators of osteoclasts control bone homeostasis under physiological and pathological conditions in mouse modelsR01AR070135 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2017 to 2021
$1.6M
Cbfβ mediates articular cartilage regeneration and repair in agingR56AG056438 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2017 to 2017
$371k
National Natural Science Foundation of China (National Science Foundation of China) 81772017National Natural Science Foundation of China (National Science Foundation of China) 82072106NIAMS NIH HHS R01 AR070135NIAMS NIH HHS R01 AR074954NIAMS NIH HHS R01 AR075735NIA NIH HHS R01 AG056438NIA NIH HHS R56 AG056438NIDCR NIH HHS R01 DE023813NIDCR NIH HHS R01 DE028264U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) AR070135U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) AR074954U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) AR075735U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) DE023813U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) DE028264U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) AG056438
6 · The paper itself

Abstract

Wnts are secreted, lipid-modified proteins that bind to different receptors on the cell surface to activate canonical or non-canonical Wnt signaling pathways, which control various biological processes throughout embryonic development and adult life. Aberrant Wnt signaling pathway underlies a wide range of human disease pathogeneses. In this review, we provide an update of Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and diseases. The Wnt proteins, receptors, activators, inhibitors, and the crosstalk of Wnt signaling pathways with other signaling pathways are summarized and discussed. We mainly review Wnt signaling functions in bone formation, homeostasis, and related diseases, and summarize mouse models carrying genetic modifications of Wnt signaling components. Moreover, the therapeutic strategies for treating bone diseases by targeting Wnt signaling, including the extracellular molecules, cytosol components, and nuclear components of Wnt signaling are reviewed. In summary, this paper reviews our current understanding of the mechanisms by which Wnt signaling regulates bone formation, homeostasis, and the efforts targeting Wnt signaling for treating bone diseases. Finally, the paper evaluates the important questions in Wnt signaling to be further explored based on the progress of new biological analytical technologies.

Indexed as

Bone DiseasesHomeostasisOsteogenesisWnt Signaling PathwayAnimalsbeta CateninHumansWnt Proteinsbeta CateninWnt Proteins

Identifiers

PMID38987555
PMCPMC11237130

What OpenQuestion 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 OpenQuestion graph.