Evidence map›Paper›PMID 21483870›Full record

ArticlePloS one2011

Activated protein synthesis and suppressed protein breakdown signaling in skeletal muscle of critically ill patients.

Jakob G Jespersen, Anders Nedergaard, Søren Reitelseder, Ulla R Mikkelsen, Kasper J Dideriksen, Jakob Agergaard, Frederik Kreiner, Frank C Pott, Peter Schjerling, Michael Kjaer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Molecular mechanisms of postintensive care syndrome.Intensive care medicine experimental · 2021
    Review
  12. Molecular Mechanisms of Muscle Fatigue.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Bioinformatics Analysis Identifies Hub Genes and Molecular Pathways Involved in Sepsis-Induced Myopathy.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Regulation of muscle protein synthesis and the effects of catabolic states.The international journal of biochemistry & cell biology · 2013
    Review
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

10 authors at 3 institutions in 1 country.

Jakob G JespersenDepartment of Orthopedic Surgery M, Institute of Sports Medicine Copenhagen, Bispebjerg Hospital and Center for Healthy Aging, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. jespersen.jakob@gmail.com
Anders Nedergaard
Søren Reitelseder
Ulla R Mikkelsen
Kasper J Dideriksen
Jakob Agergaard
Frederik Kreiner
Frank C Pott
Peter Schjerling
Michael Kjaer
Bispebjerg Hospital · DKUniversity of Copenhagen · DKRigshospitalet · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSkeletal muscle mass is controlled by myostatin and Akt-dependent signaling on mammalian target of rapamycin (mTOR), glycogen synthase kinase 3β (GSK3β) and forkhead box O (FoxO) pathways, but it is unknown how these pathways are regulated in critically ill human muscle. To describe factors involved in muscle mass regulation, we investigated the phosphorylation and expression of key factors in these protein synthesis and breakdown signaling pathways in thigh skeletal muscle of critically ill intensive care unit (ICU) patients compared with healthy controls. METHODOLOGY/PRINCIPAL

findingsICU patients were systemically inflamed, moderately hyperglycemic, received insulin therapy, and showed a tendency to lower plasma branched chain amino acids compared with controls. Using Western blotting we measured Akt, GSK3β, mTOR, ribosomal protein S6 kinase (S6k), eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), and muscle ring finger protein 1 (MuRF1); and by RT-PCR we determined mRNA expression of, among others, insulin-like growth factor 1 (IGF-1), FoxO 1, 3 and 4, atrogin1, MuRF1, interleukin-6 (IL-6), tumor necrosis factor α (TNF-α) and myostatin. Unexpectedly, in critically ill ICU patients Akt-mTOR-S6k signaling was substantially higher compared with controls. FoxO1 mRNA was higher in patients, whereas FoxO3, atrogin1 and myostatin mRNAs and MuRF1 protein were lower compared with controls. A moderate correlation (r2=0.36, p<0.05) between insulin infusion dose and phosphorylated Akt was demonstrated. CONCLUSIONS/SIGNIFICANCE: We present for the first time muscle protein turnover signaling in critically ill ICU patients, and we show signaling pathway activity towards a stimulation of muscle protein synthesis and a somewhat inhibited proteolysis.

Indexed as

Critical IllnessAdultAgedBlotting, WesternCase-Control StudiesFemaleHumansMaleMiddle AgedMuscle ProteinsMuscle, SkeletalProtein BiosynthesisReverse Transcriptase Polymerase Chain ReactionSignal TransductionMuscle Proteins

Identifiers

PMID21483870
PMCPMC3069050
OpenAlexW2091837818

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.