Evidence map›Paper›PMID 40362247›Full record

ReviewInternational journal of molecular sciences2025

Mechanosignaling in Osteoporosis: When Cells Feel the Force.

Nuo Chen, Marina Danalache, Chen Liang, Dorothea Alexander, Felix Umrath

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Ciliary-Mediated Mechanotransduction in Skeletal Development and Diseases.Results and problems in cell differentiation · 2026
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
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

5 authors.

Nuo ChenDepartment of Orthopedic Surgery, University Hospital Tübingen, 72072 Tübingen, Germany.
Marina DanalacheDepartment of Orthopedic Surgery, University Hospital Tübingen, 72072 Tübingen, Germany.
Chen LiangDepartment of Orthopedic Surgery, University Hospital Tübingen, 72072 Tübingen, Germany.ORCID 0000-0002-4866-8064
Dorothea AlexanderDepartment of Oral and Maxillofacial Surgery, University Hospital Tübingen, 72076 Tübingen, Germany.
Felix UmrathDepartment of Orthopedic Surgery, University Hospital Tübingen, 72072 Tübingen, Germany.ORCID 0000-0003-2040-7492

Funding

China Scholarship Council 202408080033
6 · The paper itself

Abstract

Bone is a highly mechanosensitive tissue, where mechanical signaling plays a central role in maintaining skeletal homeostasis. Mechanotransduction regulates the balance between bone formation and resorption through coordinated interactions among bone cells. Key mechanosensing structures-including the extracellular/pericellular matrix (ECM/PCM), integrins, ion channels, connexins, and primary cilia, translate mechanical cues into biochemical signals that drive bone adaptation. Disruptions in mechanotransduction are increasingly recognized as an important factor in osteoporosis. Under pathological conditions, impaired mechanical signaling reduces bone formation and accelerates bone resorption, leading to skeletal fragility. Defects in mechanotransduction disrupt key pathways involved in bone metabolism, further exacerbating bone loss. Therefore, targeting mechanotransduction presents a promising pharmacological strategy for osteoporosis treatment. Recent advances have focused on developing drugs that enhance bone mechanosensitivity by modulating key mechanotransduction pathways, including integrins, ion channels, connexins, and Wnt signaling. A deeper understanding of mechanosignaling mechanisms may pave the way for novel therapeutic approaches aimed at restoring bone mass, mechanical integrity, and mechanosensitive bone adaptation.

Indexed as

Mechanotransduction, CellularOsteoporosisAnimalsBone and BonesExtracellular MatrixHumansIntegrinsIon ChannelsOsteogenesisIntegrinsIon Channelsmechanosensitive ion channelsmechanosignalingmechanotransductionosteoporosissecondary osteoporosis

Identifiers

PMID40362247
PMCPMC12071322

What OpenQuestion holds

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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.