Evidence map›Paper›PMID 37694373›Full record

ReviewJournal of neuromuscular diseases2023

Towards the Identification of Biomarkers for Muscle Function Improvement in Myotonic Dystrophy Type 1.

Amira Aoussim, Cécilia Légaré, Marie-Pier Roussel, Anne-Marie Madore, Mathieu C Morissette, Catherine Laprise, Elise Duchesne

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neuromuscular diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  5. Article
  6. Article
  7. 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

7 authors at 2 institutions in 2 countries.

Amira AoussimDépartement des sciences de la santé, Université du Québec à Chicoutimi, Québec, Canada.
Cécilia LégaréDépartement des sciences de la santé, Université du Québec à Chicoutimi, Québec, Canada.
Marie-Pier RousselGroupe de recherche interdisciplinaire sur les maladies neuromusculaires (GRIMN), Centre intégré universitaire de santé et de services sociaux du Saguenay- Lac-Saint-Jean, Hôpital de Jonquière, Québec, Canada.
Anne-Marie MadoreCentre intersectoriel en santé durable (CISD), Université du Québec à Chicoutimi, Québec, Canada.
Mathieu C MorissetteDepartment of Medicine, Université Laval, Québec, Canada.
Catherine LapriseCentre intersectoriel en santé durable (CISD), Université du Québec à Chicoutimi, Québec, Canada.
Elise DuchesneDépartement des sciences de la santé, Université du Québec à Chicoutimi, Québec, Canada.
Université du Québec à Chicoutimi · CAUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyotonic dystrophy type 1 (DM1) is the most common muscular dystrophy in adults. In DM1 patients, skeletal muscle is severely impaired, even atrophied and patients experience a progressive decrease in maximum strength. Strength training for these individuals can improve their muscle function and mass, however, the biological processes involved in these improvements remain unknown.

objectiveThis exploratory study aims at identifying the proteomic biomarkers and variables associated with the muscle proteome changes induced by training in DM1 individuals.

methodsAn ion library was developed from liquid chromatography-tandem mass spectrometry proteomic analyses of Vastus Lateralis muscle biopsies collected in 11 individuals with DM1 pre-and post-training.

resultsThe proteomic analysis showed that the levels of 44 proteins were significantly modulated. A literature review (PubMed, UniProt, PANTHER, REACTOME) classified these proteins into biological sub-classes linked to training-induced response, including immunity, energy metabolism, apoptosis, insulin signaling, myogenesis and muscle contraction. Linear models identified key variables explaining the proteome modulation, including atrophy and hypertrophy factors. Finally, six proteins of interest involved in myogenesis, muscle contraction and insulin signaling were identified: calpain-3 (CAN3; Muscle development, positive regulation of satellite cell activation), 14-3-3 protein epsilon (1433E; Insulin/Insulin-like growth factor, PI3K/Akt signaling), myosin-binding protein H (MYBPH; Regulation of striated muscle contraction), four and a half LIM domains protein 3 (FHL3; Muscle organ development), filamin-C (FLNC; Muscle fiber development) and Cysteine and glycine-rich protein 3 (CSRP3).

conclusionThese findings may lead to the identification for DM1 individuals of novel muscle biomarkers for clinical improvement induced by rehabilitation, which could eventually be used in combination with a targeted pharmaceutical approach to improving muscle function, but further studies are needed to confirm those results.

Indexed as

InsulinsMuscular DiseasesMyotonic DystrophyAdultBiomarkersHumansMuscle, SkeletalPhosphatidylinositol 3-KinasesProteomeProteomicsBiomarkersInsulinsPhosphatidylinositol 3-KinasesProteomeMyotonic dystrophyproteomicsstrength training

Identifiers

PMID37694373
PMCPMC10657677
OpenAlexW4386465574

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.