Evidence map›Paper›PMID 23389618›Full record

ReviewNature medicine2013

WNT signaling in bone homeostasis and disease: from human mutations to treatments.

Roland Baron, Michaela Kneissel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,114 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,114citing papers in PubMed, 4 pooled it
74.0field-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

1,114 citing papers in PubMed, 4 syntheses or guidelines pooled it, 2,033 citations in OpenAlex.

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1,054 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 at 2 institutions in 2 countries.

Roland BaronDepartment of Medicine, Harvard Medical School, Harvard University, Boston, Massachusetts, USA. roland_baron@hsdm.harvard.edu
Michaela Kneissel
Harvard University · USNovartis Institutes for BioMedical Research

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low bone mass and strength lead to fragility fractures, for example, in elderly individuals affected by osteoporosis or children with osteogenesis imperfecta. A decade ago, rare human mutations affecting bone negatively (osteoporosis-pseudoglioma syndrome) or positively (high-bone mass phenotype, sclerosteosis and Van Buchem disease) have been identified and found to all reside in components of the canonical WNT signaling machinery. Mouse genetics confirmed the importance of canonical Wnt signaling in the regulation of bone homeostasis, with activation of the pathway leading to increased, and inhibition leading to decreased, bone mass and strength. The importance of WNT signaling for bone has also been highlighted since then in the general population in numerous genome-wide association studies. The pathway is now the target for therapeutic intervention to restore bone strength in millions of patients at risk for fracture. This paper reviews our current understanding of the mechanisms by which WNT signalng regulates bone homeostasis.

Indexed as

HomeostasisMutationAnimalsbeta CateninBone and BonesBone DensityBone DevelopmentBone Morphogenetic ProteinsHematopoiesisHumansLow Density Lipoprotein Receptor-Related Protein-5Low Density Lipoprotein Receptor-Related Protein-6MiceWnt Signaling Pathwaybeta CateninBone Morphogenetic ProteinsLow Density Lipoprotein Receptor-Related Protein-5Low Density Lipoprotein Receptor-Related Protein-6LRP5 protein, humanLRP6 protein, human

Identifiers

PMID23389618
OpenAlexW2019196925

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.