Evidence map›Paper›PMID 29046370›Full record

ArticleBioscience reports2017

Excessive glucocorticoid-induced muscle MuRF1 overexpression is independent of Akt/FoXO1 pathway.

Xiao Juan Wang, Jing Jing Xiao, Lei Liu, Hong Chao Jiao, Hai Lin

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

Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

18 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Puerarin-RichPreventive nutrition and food science · 2026
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  4. Review
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  14. Article
  15. Review
  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
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.

Xiao Juan WangShandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science, Shandong Agricultural University, 61 Daizong Street, Taian City, Shandong Province 271018, China.
Jing Jing XiaoShandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science, Shandong Agricultural University, 61 Daizong Street, Taian City, Shandong Province 271018, China.
Lei LiuShandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science, Shandong Agricultural University, 61 Daizong Street, Taian City, Shandong Province 271018, China.
Hong Chao JiaoShandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science, Shandong Agricultural University, 61 Daizong Street, Taian City, Shandong Province 271018, China.
Hai LinShandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science, Shandong Agricultural University, 61 Daizong Street, Taian City, Shandong Province 271018, China hailin@sdau.edu.cn.
Shandong Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ubiquitin-proteasome system (UPS)-dependent proteolysis plays a major role in the muscle catabolic action of glucocorticoids (GCs). Atrogin-1 and muscle-specific RING finger protein 1 (MuRF1), two E3 ubiquitin ligases, are uniquely expressed in muscle. It has been previously demonstrated that GC treatment induced MuRF1 and atrogin-1 overexpression. However, it is yet unclear whether the higher pharmacological dose of GCs induced muscle protein catabolism through MuRF1 and atrogin-1. In the present study, the role of atrogin-1 and MuRF1 in C2C12 cells protein metabolism during excessive dexamethasone (DEX) was studied. The involvement of Akt/forkhead box O1 (FoXO1) signaling pathway and the cross-talk between anabolic regulator mammalian target of rapamycin (mTOR) and catabolic regulator FoXO1 were investigated. High concentration of DEX increased MuRF1 protein level in a time-dependent fashion (

Indexed as

ProteolysisAnimalsCell LineChromonesDexamethasoneEnzyme InhibitorsForkhead Box Protein O1GlucocorticoidsHormone AntagonistsMiceMifepristoneMorpholinesMuscle ProteinsMuscle, SkeletalPhosphorylationProteasome Endopeptidase Complex2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAkt1 protein, mouseChromonesDexamethasoneEnzyme InhibitorsFbxo32 protein, mouseForkhead Box Protein O1Foxo1 protein, mouseGlucocorticoidsHormone AntagonistsMifepristoneMorpholinesmTOR protein, mouseMuscle ProteinsProteasome Endopeptidase ComplexProteasome InhibitorsProto-Oncogene Proteins c-aktSirolimusSKP Cullin F-Box Protein LigasesTOR Serine-Threonine KinasesTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesFoXO1glucocorticoidMuRF1muscle cellprotein metabolism

Identifiers

PMID29046370
PMCPMC5691142
OpenAlexW2766656449

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.