Evidence map›Paper›PMID 23815527›Full record

ReviewAntioxidants & redox signaling2014

Mechanosignaling in bone health, trauma and inflammation.

Derrick M Knapik, Priyangi Perera, Jin Nam, Alisa D Blazek, Björn Rath, Binnaz Leblebicioglu, Hiranmoy Das, Lai Chu Wu, Timothy E Hewett, Suresh K Agarwal and 4 more

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. [Osteoarthritis and cartilage · 2022
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Network Pharmacological Study ofBioMed research international · 2021
    Article
  17. NF-κB inhibitor, NEMO-binding domain peptide attenuates intervertebral disc degeneration.The spine journal : official journal of the North American Spine Society · 2020
    Article
  18. Article
  19. Mechanotransduction in Wound Healing and Fibrosis.Journal of clinical medicine · 2020
    Review
  20. 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

14 authors.

Derrick M Knapik1 Department of Orthopaedic Surgery, The Ohio State University College of Medicine , Columbus, Ohio.
Priyangi Perera
Jin Nam
Alisa D Blazek
Björn Rath
Binnaz Leblebicioglu
Hiranmoy Das
Lai Chu Wu
Timothy E Hewett
Suresh K Agarwal
Alexander G Robling
David C Flanigan
Beth S Lee
Sudha Agarwal

Funding

Comprehensive Training in Oral &Craniofacial SciencesT32DE014320 · NIDCR · OHIO STATE UNIVERSITY · PI SHERIDAN, JOHN F · 2001 to 2022
$10.2M
Lrp5 signaling in bone mechanotransduction and metabolismR01AR053237 · NIAMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI ALEXANDER G ROBLING, Matthew L Warman · 2005 to 2026
$9.4M
Exercise Driven Molecular Mechanisms of Joint RepairR01AR048781 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2002 to 2006
$1.5M
NIAMS NIH HHS AR48781NIAMS NIH HHS R01 AR053237NIDCR NIH HHS DE014320NIDCR NIH HHS DE105399
6 · The paper itself

Abstract

significanceMechanosignaling is vital for maintaining the structural integrity of bone under physiologic conditions. These signals activate and suppress multiple signaling cascades regulating bone formation and resorption. Understanding these pathways is of prime importance to exploit their therapeutic potential in disorders associated with bone loss due to disuse, trauma, or disruption of homeostatic mechanisms. RECENT ADVANCES: In the case of cells of the bone, an impressive amount of data has been generated that provides evidence of a complex mechanism by which mechanical signals can maintain or disrupt cellular homeostasis by driving transcriptional regulation of growth factors, matrix proteins and inflammatory mediators in health and inflammation. Mechanical signals act on cells in a magnitude dependent manner to induce bone deposition or resorption. During health, physiological levels of these signals are essential for maintaining bone strength and architecture, whereas during inflammation, similar signals can curb inflammation by suppressing the nuclear factor kappa B (NF-κB) signaling cascade, while upregulating matrix synthesis via mothers against decapentaplegic homolog and/or Wnt signaling cascades. Contrarily, excessive mechanical forces can induce inflammation via activation of the NF-κB signaling cascade. CRITICAL ISSUES: Given the osteogenic potential of mechanical signals, it is imperative to exploit their therapeutic efficacy for the treatment of bone disorders. Here we review select signaling pathways and mediators stimulated by mechanical signals to modulate the strength and integrity of the bone. FUTURE DIRECTIONS: Understanding the mechanisms of mechanotransduction and its effects on bone lay the groundwork for development of nonpharmacologic mechanostimulatory approaches for osteodegenerative diseases and optimal bone health.

Indexed as

AnimalsBone and BonesHumansInflammationMechanotransduction, CellularNF-kappa BWounds and InjuriesNF-kappa B

Identifiers

PMID23815527
PMCPMC3924811

What OpenQuestion holds

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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.