Evidence map›Paper›PMID 28359087›Full record

ArticleEndocrinology2017

Glucocorticoids Induce Bone and Muscle Atrophy by Tissue-Specific Mechanisms Upstream of E3 Ubiquitin Ligases.

Amy Y Sato, Danielle Richardson, Meloney Cregor, Hannah M Davis, Ernie D Au, Kevin McAndrews, Teresa A Zimmers, Jason M Organ, Munro Peacock, Lilian I Plotkin and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 6 pooled it
5.3field-weighted citation impact, top 3% 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

87 citing papers in PubMed, 6 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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27 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

11 authors at 4 institutions in 1 country.

Amy Y SatoDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Danielle RichardsonDepartment 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.
Hannah M DavisDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Ernie D AuIndiana Center for Musculoskeletal Health, Indianapolis, Indiana.
Kevin McAndrewsDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Teresa A ZimmersDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Jason M OrganDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Munro PeacockIndiana Center for Musculoskeletal Health, Indianapolis, Indiana.
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.
Indiana Hemophilia and Thrombosis Center · USIndiana University – Purdue University Indianapolis · USIndiana University School of MedicineRichard L. Roudebush VA Medical Center · US

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
Physiologic Regulation of Hematopoiesis by NotchR01DK097837 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI CARLESSO, NADIA · 2014 to 2017
$1.6M
Manipulation of STAT3 Signaling for Muscle Preservation in Cancer CachexiaR01CA122596 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ZIMMERS, TERESA A · 2010 to 2015
$1.6M
Myostatin Family Signaling in Burn-Injury Related Muscle WastingR01GM092758 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ZIMMERS, TERESA A · 2010 to 2014
$1.6M
PQB3: Mechanisms & Targeting of Sonic Hedgehog Signaling in Muscle Wasting of Cancer CachexiaR01CA194593 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI ZIMMERS, TERESA A · 2015 to 2018
$1.4M
PTH receptor Signaling and Diabetes-induced Bone DiseaseI01BX002104 · VA · RLR VA MEDICAL CENTER · PI BELLIDO, TERESITA M. · 2014 to 2023
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BLRD VA I01 BX002104NCI NIH HHS R01 CA122596NCI NIH HHS R01 CA194593NHLBI NIH HHS T35 HL110854NIAMS NIH HHS R01 AR059357NIAMS NIH HHS T32 AR065971NIDDK NIH HHS R01 DK097837NIGMS NIH HHS R01 GM092758
6 · The paper itself

Abstract

Glucocorticoid excess, either endogenous with diseases of the adrenal gland, stress, or aging or when administered for immunosuppression, induces bone and muscle loss, leading to osteopenia and sarcopenia. Muscle weakness increases the propensity for falling, which, combined with the lower bone mass, increases the fracture risk. The mechanisms underlying glucocorticoid-induced bone and muscle atrophy are not completely understood. We have demonstrated that the loss of bone and muscle mass, decreased bone formation, and reduced muscle strength, hallmarks of glucocorticoid excess, are accompanied by upregulation in both tissues in vivo of the atrophy-related genes atrogin1, MuRF1, and MUSA1. These are E3 ubiquitin ligases traditionally considered muscle-specific. Glucocorticoids also upregulated atrophy genes in cultured osteoblastic/osteocytic cells, in ex vivo bone organ cultures, and in muscle organ cultures and C2C12 myoblasts/myotubes. Furthermore, glucocorticoids markedly increased the expression of components of the Notch signaling pathway in muscle in vivo, ex vivo, and in vitro. In contrast, glucocorticoids did not increase Notch signaling in bone or bone cells. Moreover, the increased expression of atrophy-related genes in muscle, but not in bone, and the decreased myotube diameter induced by glucocorticoids were prevented by inhibiting Notch signaling. Thus, glucocorticoids activate different mechanisms in bone and muscle that upregulate atrophy-related genes. However, the role of these genes in the effects of glucocorticoids in bone is unknown. Nevertheless, these findings advance our knowledge of the mechanism of action of glucocorticoids in the musculoskeletal system and provide the basis for novel therapies to prevent glucocorticoid-induced atrophy of bone and muscle.

Indexed as

AnimalsBone and BonesCells, CulturedFemaleGene ExpressionGlucocorticoidsMice, Inbred C57BLMuscle, SkeletalMuscular AtrophyOsteoblastsOsteoclastsRandom AllocationReceptors, NotchSignal TransductionUbiquitin-Protein LigasesGlucocorticoidsReceptors, NotchUbiquitin-Protein Ligases

Identifiers

PMID28359087
PMCPMC5460781
OpenAlexW2619897119

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.