Evidence map›Paper›PMID 27713817›Full record

ArticleSkeletal muscle2016

VAChT overexpression increases acetylcholine at the synaptic cleft and accelerates aging of neuromuscular junctions.

Satoshi Sugita, Leland L Fleming, Caleb Wood, Sydney K Vaughan, Matheus P S M Gomes, Wallace Camargo, Ligia A Naves, Vania F Prado, Marco A M Prado, Cristina Guatimosim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
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

39 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Exogenous nanomolar zinc ion (ZnBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Sex-dependent cholinergic effects on amyloid pathology: A translational study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

11 authors at 4 institutions in 3 countries.

Satoshi SugitaVirginia Tech Carilion Research Institute, Virginia Tech, Roanoke, VA USA.
Leland L FlemingVirginia Tech Carilion Research Institute, Virginia Tech, Roanoke, VA USA ; Virginia Tech Postbaccalaureate Research and Education (VT PREP) Scholar, Virginia Tech, Blacksburg, VA USA.
Caleb WoodVirginia Tech Carilion Research Institute, Virginia Tech, Roanoke, VA USA.
Sydney K VaughanVirginia Tech Carilion Research Institute, Virginia Tech, Roanoke, VA USA ; Graduate Program in Translational Biology, Medicine, and Health, Virginia Tech, Blacksburg, VA USA.
Matheus P S M GomesDepartamento de Morfologia, Instiuto Ciencias Biologicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais Brazil.
Wallace CamargoDepartamento de Fisiologia e Biofísica, Instiuto Ciencias Biologicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais Brazil.
Ligia A NavesDepartamento de Fisiologia e Biofísica, Instiuto Ciencias Biologicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais Brazil.
Vania F PradoRobarts Research Institute, Department of Physiology and Pharmacology, Department of Anatomy & Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON N6A5K8 Canada.
Marco A M PradoRobarts Research Institute, Department of Physiology and Pharmacology, Department of Anatomy & Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON N6A5K8 Canada.
Cristina GuatimosimDepartamento de Morfologia, Instiuto Ciencias Biologicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais Brazil.
Gregorio ValdezVirginia Tech Carilion Research Institute, Virginia Tech, Roanoke, VA USA ; Department of Biological Sciences, Virginia Tech, Blacksburg, VA USA.ORCID 0000-0002-0375-4532
Universidade Federal de Minas Gerais · BRCarilion Clinic · USVirginia Tech - Wake Forest University School of Biomedical Engineering & Sciences · USWestern University · CA

Funding

VT Post Baccalaureate Research and Education ProgramR25GM066534 · NIGMS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SMITH, EDWARD J · 2003 to 2024
$7.6M
Role of Target-derived FGFs in Maintaining and Repairing SynapsesK01NS085071 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI VALDEZ, GREGORIO · 2013 to 2015
$679k
Synaptic FGFs are required and sufficient to maintain and repair aged NMJsR56AG051501 · NIA · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI VALDEZ, GREGORIO · 2015 to 2015
$377k
NIA NIH HHS R56 AG051501NIGMS NIH HHS R25 GM066534NINDS NIH HHS K01 NS085071
6 · The paper itself

Abstract

backgroundCholinergic dysfunction occurs during aging and in a variety of diseases, including amyotrophic lateral sclerosis (ALS). However, it remains unknown whether changes in cholinergic transmission contributes to age- and disease-related degeneration of the motor system. Here we investigated the effect of moderately increasing levels of synaptic acetylcholine (ACh) on the neuromuscular junction (NMJ), muscle fibers, and motor neurons during development and aging and in a mouse model for amyotrophic lateral sclerosis (ALS).

methodsChat-ChR2-EYFP (VAChT

resultsWe show that VAChT is elevated in the spinal cord and at NMJs of VAChT

conclusionsThe data presented in this manuscript demonstrate that increasing levels of ACh at the synaptic cleft promote degeneration of adult NMJs, contributing to age- and disease-related motor deficits. We thus propose that maintaining normal cholinergic signaling in muscles will slow degeneration of NMJs and attenuate loss of motor function caused by aging and neuromuscular diseases.

Indexed as

AgingAcetylcholineAmyotrophic Lateral SclerosisAnimalsDisease Models, AnimalFemaleMaleMiceMice, TransgenicMiniature Postsynaptic PotentialsMotor NeuronsMuscle, SkeletalNeuromuscular JunctionRNA, MessengerSpinal CordSurvival AnalysisAcetylcholineRNA, MessengerSlc18a3 protein, mouseVesicular Acetylcholine Transport ProteinsAcetylcholineAgingALSCholinergic transmissionMotor neuronNeuromuscular junctionSynapseVAChT

Identifiers

PMID27713817
PMCPMC5050580
OpenAlexW2529504904

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.