Evidence map›Paper›PMID 16361069›Full record

ReviewGene2006

Molecular pathways mediating mechanical signaling in bone.

Janet Rubin, Clinton Rubin, Christopher Rae Jacobs

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed
13.8field-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

170 citing papers in PubMed, 476 citations in OpenAlex.

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  20. Up-to-date progress in bioprinting of bone tissue.International journal of bioprinting · 2023
    Review

110 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.

Janet RubinDepartment of Medicine, VAMC and Emory University School of Medicine, Atlanta GA, VAMC-151, 1670 Clairmont Rd, Decatur, GA 30033, USA. janet.rubin@emory.edu
Clinton Rubin
Christopher Rae Jacobs
Emory University · USStanford University · USStony Brook University · US

Funding

UNDERSTANDING AND IMPROVING SMALL MOLECULE INHIBITORS OF PRION REPLICATIONP01AG021601 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PRUSINER, STANLEY B · 2003 to 2013
$31.9M
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
MECHANOTRANSDUCTION IN BONE VIA OSCILLATING FLUID FLOWR01AR045989 · NIAMS · STANFORD UNIVERSITY · PI JACOBS, CHRISTOPHER RAE · 2000 to 2009
$2.4M
ORGANIZATION OF MECHANICAL SIGNALS VIA MEMBRANE SCAFFOLDR01AR052014 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUBIN, JANET E · 2005 to 2008
$1.1M
Biophysical regulation of bone remodelingR56AR042360 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUBIN, JANET E · 2008 to 2008
$289k
NIAMS NIH HHS AR42360NIAMS NIH HHS AR43498NIAMS NIH HHS AR45989NIAMS NIH HHS R01 AR042360NIAMS NIH HHS R01 AR043498NIAMS NIH HHS R01 AR045989NIAMS NIH HHS R01 AR052014NIAMS NIH HHS R56 AR042360NIA NIH HHS P01 AG021601
6 · The paper itself

Abstract

Bone tissue has the capacity to adapt to its functional environment such that its morphology is "optimized" for the mechanical demand. The adaptive nature of the skeleton poses an interesting set of biological questions (e.g., how does bone sense mechanical signals, what cells are the sensing system, what are the mechanical signals that drive the system, what receptors are responsible for transducing the mechanical signal, what are the molecular responses to the mechanical stimuli). Studies of the characteristics of the mechanical environment at the cellular level, the forces that bone cells recognize, and the integrated cellular responses are providing new information at an accelerating speed. This review first considers the mechanical factors that are generated by loading in the skeleton, including strain, stress and pressure. Mechanosensitive cells placed to recognize these forces in the skeleton, osteoblasts, osteoclasts, osteocytes and cells of the vasculature are reviewed. The identity of the mechanoreceptor(s) is approached, with consideration of ion channels, integrins, connexins, the lipid membrane including caveolar and non-caveolar lipid rafts and the possibility that altering cell shape at the membrane or cytoskeleton alters integral signaling protein associations. The distal intracellular signaling systems on-line after the mechanoreceptor is activated are reviewed, including those emanating from G-proteins (e.g., intracellular calcium shifts), MAPKs, and nitric oxide. The ability to harness mechanical signals to improve bone health through devices and exercise is broached. Increased appreciation of the importance of the mechanical environment in regulating and determining the structural efficacy of the skeleton makes this an exciting time for further exploration of this area.

Indexed as

Signal TransductionAnimalsBiomechanical PhenomenaBone and BonesConnexinsHumansIon ChannelsMembrane MicrodomainsModels, BiologicalNitric Oxide SynthaseOsteoblastsOsteoclastsOsteocytesConnexinsIon ChannelsNitric Oxide Synthase

Identifiers

PMID16361069
PMCPMC3687520
OpenAlexW2108704056

What OpenQuestion holds

Textmetadata
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.