Evidence map›Paper›PMID 19817708›Full record

ReviewCritical reviews in eukaryotic gene expression2009

Mechanical signaling for bone modeling and remodeling.

Alexander G Robling, Charles H Turner

Abstract readReview
In one paragraph

Review in Critical reviews in eukaryotic gene expression, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing 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

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

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  13. Palatal Osteogenesis After Cleft Palatoplasty: Does the Bone Grow?The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association · 2026
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153 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

2 authors.

Alexander G RoblingDepartment of Anatomy, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Charles H Turner

Funding

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
GENETIC ANALYSIS OF VERTEBRAL STRENGTHR01AR046530 · NIAMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI TURNER, CHARLES H · 2000 to 2008
$3.4M
Lrp5 and Lrp6 signaling in bone mechanotransduction and metabolismR56AR053237 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI ROBLING, ALEXANDER G, WARMAN, MATTHEW L · 2023 to 2023
$349k
NIAMS NIH HHS AR046530NIAMS NIH HHS AR053237NIAMS NIH HHS R01 AR046530NIAMS NIH HHS R01 AR053237NIAMS NIH HHS R56 AR053237
6 · The paper itself

Abstract

Proper development of the skeleton in utero and during growth requires mechanical stimulation. Loading results in adaptive changes in bone that strengthen bone structure. Bone's adaptive response is regulated by the ability of resident bone cells to perceive and translate mechanical energy into a cascade of structural and biochemical changes within the cells a process known as mechanotransduction. Mechanotransduction pathways are among the most anabolic in bone, and consequently, there is great interest in elucidating how mechanical loading produces its observed effects, including increased bone formation, reduced bone loss, changes in bone cell differentiation and lifespan, among others. A molecular understanding of these processes is developing, and with it comes a profound new insight into the biology of bone. In this article, we review the nature of the physical stimulus to which bone cells mount an adaptive response, including the identity of the sensor cells, their attributes and physical environment, and putative mechanoreceptors they express. Particular attention is allotted to the focal adhesion and Wnt signaling, in light of their emerging role in bone mechanotransduction. Te cellular mechanisms for increased bone loss during disuse, and reduced bone loss during loading are considered. Finally, we summarize the published data on bone cell accommodation, whereby bone cells stop responding to mechanical signaling events. Collectively, these data highlight the complex yet finely orchestrated process of mechanically regulated bone homeostasis.

Indexed as

Bone RemodelingAnimalsBiomechanical PhenomenaBone and BonesBone DensityBone ResorptionHumansLDL-Receptor Related ProteinsLow Density Lipoprotein Receptor-Related Protein-5Mechanotransduction, CellularOsteoblastsOsteogenesisSignal TransductionStress, MechanicalWnt ProteinsLDL-Receptor Related ProteinsLow Density Lipoprotein Receptor-Related Protein-5LRP5 protein, humanWnt Proteins

Identifiers

PMID19817708
PMCPMC3743123

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.