Evidence map›Paper›PMID 26870889›Full record

ReviewCurrent opinion in clinical nutrition and metabolic care2016

Neuromuscular junction degeneration in muscle wasting.

Rüdiger Rudolf, Michael R Deschenes, Marco Sandri

Open access · hybridAbstract readReview
In one paragraph

Review in Current opinion in clinical nutrition and metabolic care, 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
2.6field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  12. Emerging role of TAK1 in the regulation of skeletal muscle mass.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Review
  13. Critical Illness Myopathy Alters Diaphragm Neuromuscular Junction Protein and Gene Expression.American journal of respiratory and critical care medicine · 2023
    Article
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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

3 authors at 3 institutions in 3 countries.

Rüdiger RudolfaInterdisciplinary Center for Neuroscience, University of Heidelberg, Heidelberg bInstitute of Molecular and Cell Biology, Mannheim University of Applied Science, Mannheim cInstitute of Toxicology and Genetics, Karlsruhe Institute of Technology, Karlsruhe, Germany dDepartment of Kinesiology and Health Sciences, The College of William and Mary, Williamsburg, Virginia, USA eDepartment of Biomedical Science, University of Padua fVenetian Institute of Molecular Medicine (VIMM), Padua, Italy.
Michael R Deschenes
Marco Sandri
Karlsruhe Institute of Technology · DEVeneto Institute of Molecular Medicine · ITWilliam & Mary · US

Funding

Sex specific adaptations to muscle unloadingR15AR060637 · NIAMS · COLLEGE OF WILLIAM AND MARY · PI DESCHENES, MICHAEL R · 2010 to 2010
$193k
NIAMS NIH HHS R15 AR060637PHS HHS R15 060 637
6 · The paper itself

Abstract

purpose of reviewDenervation is a hallmark of age-related and other types of muscle wasting. This review focuses on recent insights and current viewpoints regarding the mechanisms and clinical relevance of maintaining the neuromuscular junction to counteract muscle wasting resulting from aging or neural disease/damage. RECENT

findingsActivity-dependent regulation of autophagy, the agrin-muscle specific kinase-Lrp4 signaling axis, and sympathetic modulation are principal mechanisms involved in stabilizing the neuromuscular junction. These findings are derived from several animal models and were largely confirmed by human gene expression analysis as well as insights from rare neuromuscular diseases such as amyotrophic lateral sclerosis and congenital myasthenic syndromes. Based on these insights, agrin-derived fragments are currently being evaluated as biomarkers for age-related muscle wasting. Tuning of autophagy, of the agrin pathway, and of sympathetic input are being studied as clinical treatment of muscle wasting disorders. SUMMARY: Basic research has revealed that maintenance of neuromuscular junctions and a few signaling pathways are important in the context of age-dependent and other forms of muscle wasting. These findings have recently started to enter clinical practice, but further research needs to substantiate and refine our knowledge.

Indexed as

Models, BiologicalAnimalsAutophagyGene Expression RegulationHumansMuscle ProteinsMuscular AtrophyNerve DegenerationNerve Tissue ProteinsNeuromuscular JunctionNeuromuscular Junction DiseasesWasting SyndromeWnt Signaling PathwayMuscle ProteinsNerve Tissue Proteins

Identifiers

PMID26870889
PMCPMC4946244
OpenAlexW2313378893

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.