Evidence map›Paper›PMID 27163932›Full record

ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2016

Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin.

Amy Y Sato, Meloney Cregor, Jesus Delgado-Calle, Keith W Condon, Matthew R Allen, Munro Peacock, Lilian I Plotkin, Teresita Bellido

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

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7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Amy Y SatoDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Meloney CregorDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Jesus Delgado-CalleDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Keith W CondonDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Matthew R AllenDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Munro PeacockDepartment of Internal Medicine, Division of Endocrinology, Indiana University School of Medicine, Indianapolis, IN, USA.
Lilian I PlotkinDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Teresita BellidoDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA. tbellido@iupui.edu.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Comprehensive Training Program in Musculoskeletal ResearchT32AR065971 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI ALEXANDER G ROBLING · 2015 to 2026
$4.4M
Short-Term Training Program In Biomedical SciencesT35HL110854 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI Brittney-Shea Herbert, Catherine Rufatto Sears · 2012 to 2026
$3.4M
Glucocorticoid-induced Atrophy in Bone and MuscleR01AR059357 · NIAMS · UNIV OF ARKANSAS FOR MED SCIS · PI BELLIDO, TERESITA M. · 2011 to 2022
$3.4M
BLRD VA I01 BX002104BLRD VA IK6 BX004596NHLBI NIH HHS T35 HL110854NIAMS NIH HHS R01 AR059357NIAMS NIH HHS T32 AR065971
6 · The paper itself

Abstract

Excess of glucocorticoids, either due to disease or iatrogenic, increases bone resorption and decreases bone formation and is a leading cause of osteoporosis and bone fractures worldwide. Improved therapeutic strategies are sorely needed. We investigated whether activating Wnt/β-catenin signaling protects against the skeletal actions of glucocorticoids, using female mice lacking the Wnt/β-catenin antagonist and bone formation inhibitor Sost. Glucocorticoids decreased the mass, deteriorated the microarchitecture, and reduced the structural and material strength of bone in wild-type (WT), but not in Sost

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCyclin D1FemaleGlucocorticoidsGlycoproteinsIntercellular Signaling Peptides and ProteinsMiceMice, KnockoutOsteoporosisOsteoprotegerinWnt Signaling PathwayAdaptor Proteins, Signal TransducingCcnd1 protein, mouseCyclin D1GlucocorticoidsGlycoproteinsIntercellular Signaling Peptides and ProteinsOsteoprotegerinSost protein, mouseTnfrsf11b protein, mouseCORTICOSTEROIDSGENETIC ANIMAL MODELSMOLECULAR PATHWAYS - REMODELINGOSTEOPOROSISWNT/β-CATENIN/LRPS

Identifiers

PMID27163932
PMCPMC8499032
OpenAlexW2376677157

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.