Evidence map›Paper›PMID 31661460›Full record

ArticleJCI insight2019

Proteasome inhibition preserves longitudinal growth of denervated muscle and prevents neonatal neuromuscular contractures.

Sia Nikolaou, Alyssa Aw Cramer, Liangjun Hu, Qingnian Goh, Douglas P Millay, Roger Cornwall

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Sexual dimorphisms in skeletal muscle: current concepts and research horizons.Journal of applied physiology (Bethesda, Md. : 1985) · 2024
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Skeletal muscle fibers count on nuclear numbers for growth.Seminars in cell & developmental biology · 2021
    Review
  10. Article
  11. Timing of proteasome inhibition as a pharmacologic strategy for prevention of muscle contractures in neonatal brachial plexus injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

Sia NikolaouDivision of Orthopaedic Surgery, and.
Alyssa Aw CramerDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Liangjun HuDivision of Orthopaedic Surgery, and.
Qingnian GohDivision of Orthopaedic Surgery, and.
Douglas P MillayDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Roger CornwallDivision of Orthopaedic Surgery, and.
Cincinnati Children's Hospital Medical Center · US

Funding

Deciphering mechanisms of myoblast fusionR01AR068286 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI MILLAY, DOUGLAS PAUL · 2015 to 2024
$4.2M
Role of skeletal muscle stem cell fusion and fibrosis during agingR01AG059605 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI MILLAY, DOUGLAS PAUL · 2018 to 2022
$1.7M
NIAMS NIH HHS R01 AR068286NIA NIH HHS R01 AG059605
6 · The paper itself

Abstract

Muscle contractures are a prominent and disabling feature of many neuromuscular disorders, including the 2 most common forms of childhood neurologic dysfunction: neonatal brachial plexus injury (NBPI) and cerebral palsy. There are currently no treatment strategies to directly alter the contracture pathology, as the pathogenesis of these contractures is unknown. We previously showed in a mouse model of NBPI that contractures result from impaired longitudinal muscle growth. Current presumed explanations for growth impairment in contractures focus on the dysregulation of muscle stem cells, which differentiate and fuse to existing myofibers during growth, as this process has classically been thought to control muscle growth during the neonatal period. Here, we demonstrate in a mouse model of NBPI that denervation does not prevent myonuclear accretion and that reduction in myonuclear number has no effect on functional muscle length or contracture development, providing definitive evidence that altered myonuclear accretion is not a driver of neuromuscular contractures. In contrast, we observed elevated levels of protein degradation in NBPI muscle, and we demonstrate that contractures can be pharmacologically prevented with the proteasome inhibitor bortezomib. These studies provide what we believe is the first strategy to prevent neuromuscular contractures by correcting the underlying deficit in longitudinal muscle growth.

Indexed as

AnimalsAnimals, NewbornBortezomibBrachial PlexusContractureDisease Models, AnimalMembrane ProteinsMiceMice, KnockoutMuscle ProteinsMuscle, SkeletalNeuromuscular DiseasesPAX7 Transcription FactorProteasome Endopeptidase ComplexStem CellsTranscriptomeBortezomibMembrane ProteinsMuscle ProteinsPax7 protein, mousePAX7 Transcription FactorProteasome Endopeptidase ComplexMuscle BiologyNeuromuscular disease

Identifiers

PMID31661460
PMCPMC6962017
OpenAlexW2982332611

What OpenQuestion holds

Textmetadata
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.