Evidence map›Paper›PMID 22575727›Full record

ReviewGene2012

Mechanical regulation of signaling pathways in bone.

William R Thompson, Clinton T Rubin, Janet Rubin

Abstract readReview
In one paragraph

Review in Gene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed
13.1field-weighted citation impact, top 1% of its field
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

197 citing papers in PubMed, 415 citations in OpenAlex.

  1. Article
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  14. Piezoelectric Biomaterials for Bone Regeneration: Roadmap from Dipole to Osteogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  15. Article
  16. Article
  17. A mechanosensitive circuit of FAK, ROCK, and ERK controls biomineral growth and morphology in the sea urchin embryo.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Review
  19. Review
  20. Article

137 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

3 authors at 3 institutions in 1 country.

William R ThompsonDepartment of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA. wthomp@med.unc.edu
Clinton T Rubin
Janet Rubin
State University of New York · USUniversity of North Carolina at Chapel Hill · USUniversity of North Carolina Health Care · US

Funding

ELECTRIC FIELD ATTENUATION OF OSTEOCLAST FORMATIONR01AR042360 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUBIN, JANET E · 1993 to 2013
$2.8M
AUGMENTATION OF TRABECULAR BONE BY LOW MAGNITUDE STRAINR01AR043498 · NIAMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI RUBIN, CLINTON T · 1997 to 2012
$2.8M
Mechanical Control of Mesenchymal Stem Cell Lineage AllocationR01AR056655 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUBIN, JANET E · 2010 to 2014
$1.4M
Harnessing mechanical signals to control mesenchymal stem cell fateR01EB014351 · NIBIB · STATE UNIVERSITY NEW YORK STONY BROOK · PI JUDEX, STEFAN, RUBIN, CLINTON T · 2012 to 2014
$1.0M
Biophysical regulation of bone remodelingR56AR042360 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUBIN, JANET E · 2008 to 2008
$289k
NIAMS NIH HHS AR042360NIAMS NIH HHS AR043498NIAMS NIH HHS AR056655NIAMS NIH HHS R01 AR042360NIAMS NIH HHS R01 AR043498NIAMS NIH HHS R01 AR056655NIAMS NIH HHS R56 AR042360NIBIB NIH HHS R01 EB014351
6 · The paper itself

Abstract

A wide range of cell types depend on mechanically induced signals to enable appropriate physiological responses. The skeleton is particularly dependent on mechanical information to guide the resident cell population towards adaptation, maintenance and repair. Research at the organ, tissue, cell and molecular levels has improved our understanding of how the skeleton can recognize the functional environment, and how these challenges are translated into cellular information that can site-specifically alter phenotype. This review first considers those cells within the skeleton that are responsive to mechanical signals, including osteoblasts, osteoclasts, osteocytes and osteoprogenitors. This is discussed in light of a range of experimental approaches that can vary parameters such as strain, fluid shear stress, and pressure. The identity of mechanoreceptor candidates is approached, with consideration of integrins, pericellular tethers, focal adhesions, ion channels, cadherins, connexins, and the plasma membrane including caveolar and non-caveolar lipid rafts and their influence on integral signaling protein interactions. Several mechanically regulated intracellular signaling cascades are detailed including activation of kinases (Akt, MAPK, FAK), β-catenin, GTPases, and calcium signaling events. While the interaction of bone cells with their mechanical environment is complex, an understanding of mechanical regulation of bone signaling is crucial to understanding bone physiology, the etiology of diseases such as osteoporosis, and to the development of interventions to improve bone strength.

Indexed as

Signal TransductionStress, MechanicalStress, PhysiologicalBone and BonesHumansIntracellular Signaling Peptides and ProteinsMechanoreceptorsOsteoblastsOsteoclastsOsteocytesStem CellsIntracellular Signaling Peptides and Proteins

Identifiers

PMID22575727
PMCPMC3371109
OpenAlexW2003035047

What OpenQuestion holds

Textmetadata
LicenceTDM
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.