Evidence map›Paper›PMID 27742499›Full record

ReviewBone2017

Sclerostin's role in bone's adaptive response to mechanical loading.

Gabriel L Galea, Lance E Lanyon, Joanna S Price

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Bone, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 5 pooled it
5.4field-weighted citation impact, top 4% 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

81 citing papers in PubMed, 5 syntheses or guidelines pooled it, 149 citations in OpenAlex.

  1. Pooled it
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  4. The association between overweight/obesity and vertebral fractures in older adults: a meta-analysis of observational studies.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2021
    Pooled it
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  10. Review
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  17. Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025
    Review
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  20. Article

21 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 1 institution in 1 country.

Gabriel L GaleaNewlife Birth Defects Research Centre, Institute of Child Health, University College London, London WC1N 1EH, United Kingdom; School of Veterinary Sciences, University of Bristol, Langford House, Langford, Bristol BS40 5DU, United Kingdom. Electronic address: g.galea@ucl.ac.uk.
Lance E LanyonSchool of Veterinary Sciences, University of Bristol, Langford House, Langford, Bristol BS40 5DU, United Kingdom.
Joanna S PriceSchool of Veterinary Sciences, University of Bristol, Langford House, Langford, Bristol BS40 5DU, United Kingdom.
University of Bristol · GB

Funding

Wellcome TrustWellcome Trust 107474/Z/15/Z
6 · The paper itself

Abstract

Mechanical loading is the primary functional determinant of bone mass and architecture, and osteocytes play a key role in translating mechanical signals into (re)modelling responses. Although the precise mechanisms remain unclear, Wnt signalling pathway components, and the anti-osteogenic canonical Wnt inhibitor Sost/sclerostin in particular, play an important role in regulating bone's adaptive response to loading. Increases in loading-engendered strains down-regulate osteocyte sclerostin expression, whereas reduced strains, as in disuse, are associated with increased sclerostin production and bone loss. However, while sclerostin up-regulation appears to be necessary for the loss of bone with disuse, the role of sclerostin in the osteogenic response to loading is more complex. While mice unable to down-regulate sclerostin do not gain bone with loading, Sost knockout mice have an enhanced osteogenic response to loading. The molecular mechanisms by which osteocytes sense and transduce loading-related stimuli into changes in sclerostin expression remain unclear but include several, potentially interlinked, signalling cascades involving periostin/integrin, prostaglandin, estrogen receptor, calcium/NO and Igf signalling. Deciphering the mechanisms by which changes in the mechanical environment regulate sclerostin production may lead to the development of therapeutic strategies that can reverse the skeletal structural deterioration characteristic of disuse and age-related osteoporosis and enhance bones' functional adaptation to loading. By enhancing the osteogenic potential of the context in which individual therapies such as sclerostin antibodies act it may become possible to both prevent and reverse the age-related skeletal structural deterioration characteristic of osteoporosis.

Indexed as

Adaptation, PhysiologicalStress, MechanicalAnimalsBone and BonesBone Morphogenetic ProteinsOsteogenesisWeight-BearingBone Morphogenetic Proteins

Identifiers

PMID27742499
PMCPMC5340132
OpenAlexW2531453980

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.