Evidence map›Paper›PMID 27227776›Full record

ArticlePloS one2016

Glucocorticoids Enhance Muscle Proteolysis through a Myostatin-Dependent Pathway at the Early Stage.

Ruxia Wang, Hongchao Jiao, Jingpeng Zhao, Xiaojuan Wang, Hai Lin

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Article
  7. Review
  8. Review
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  12. The Roles of Androgens in Humans: Biology, Metabolic Regulation and Health.International journal of molecular sciences · 2022
    Review
  13. Article
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  15. Article
  16. Elephant seal muscle cells adapt to sustained glucocorticoid exposure by shifting their metabolic phenotype.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Observational
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

5 authors at 1 institution in 1 country.

Ruxia WangDepartment of Animal Science, Shandong Agricultural University, Shandong Key Lab for Animal Biotechnology and Disease Control, Taian, Shandong, 271018, P. R. China.
Hongchao JiaoDepartment of Animal Science, Shandong Agricultural University, Shandong Key Lab for Animal Biotechnology and Disease Control, Taian, Shandong, 271018, P. R. China.
Jingpeng ZhaoDepartment of Animal Science, Shandong Agricultural University, Shandong Key Lab for Animal Biotechnology and Disease Control, Taian, Shandong, 271018, P. R. China.
Xiaojuan WangDepartment of Animal Science, Shandong Agricultural University, Shandong Key Lab for Animal Biotechnology and Disease Control, Taian, Shandong, 271018, P. R. China.
Hai LinDepartment of Animal Science, Shandong Agricultural University, Shandong Key Lab for Animal Biotechnology and Disease Control, Taian, Shandong, 271018, P. R. China.
Shandong Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myostatin, a member of the TGF-β superfamily of secreted proteins, is expressed primarily in skeletal muscle. It negatively regulates muscle mass and is associated with glucocorticoid-induced muscle atrophy. However, it remains unclear whether myostatin is involved in glucocorticoid-induced muscle protein turnover. The aim of the present study was to investigate the role of myostatin in protein metabolism during dexamethasone (DEX) treatment. Protein synthesis rates and the expression of the genes for myostatin, ubiquitin-proteasome atrogin-1, MuRF1, FoxO1/3a and mTOR/p70S6K were determined. The results show that DEX decreased (P<0.05) protein synthesis rates while increasing the abundance of myostatin. DEX increased (P<0.05) the level of phospho-FoxO1/3a (Thr 24/32) and the expression of MuRF1. In contrast, DEX treatment had no detectable effect on atrogin-1 protein levels (P>0.05). The phosphorylation levels of mTOR and p70S6K were decreased by DEX treatment (P<0.05). Follistatin treatment inhibited the DEX-induced increase in myostatin (P<0.05) and the activation of phosphor-FoxO1/3a (Thr 24/32) (P< 0.05) and MuRF1 (P<0.05). Follistatin treatment had no influence on the protein synthesis rate or on the phosphorylation levels of mTOR (Ser 2448) and p70S6K (Thr 389) (P> 0.05). In conclusion, the present study suggests that the myostatin signalling pathway is associated with glucocorticoid-induced muscle protein catabolism at the beginning of exposure. Myostatin is not a main pathway associated with the suppression of muscle protein synthesis by glucocorticoids.

Indexed as

AnimalsCells, CulturedDexamethasoneGlucocorticoidsMyoblasts, SkeletalMyostatinPhosphorylationProteasome Endopeptidase ComplexProteolysisRibosomal Protein S6 Kinases, 70-kDaSignal TransductionTOR Serine-Threonine KinasesUbiquitinDexamethasoneGlucocorticoidsmTOR protein, mouseMyostatinProteasome Endopeptidase ComplexRibosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine KinasesUbiquitin

Identifiers

PMID27227776
PMCPMC4882021
OpenAlexW2406646548

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.