Evidence map›Paper›PMID 19656243›Full record

ReviewJournal of cellular and molecular medicine2009

Molecular events and signalling pathways involved in skeletal muscle disuse-induced atrophy and the impact of countermeasures.

Angèle Chopard, Steven Hillock, Bernard J Jasmin

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

40 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Circulating Mediators of Apoptosis and Inflammation in Aging; Physical Exercise Intervention.International journal of environmental research and public health · 2021
    Trial
  4. Trial
  5. Ets2 Is an Activity-Dependent Transcriptional Regulator of a Fast-Twitch Muscle Program.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Resistance and Aerobic Preconditioning Delays Unloading-Induced Multisystemic Physiological Changes: The NEBULA Project.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  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

3 authors at 2 institutions in 2 countries.

Angèle ChopardDepartment of Cellular and Molecular Medicine, Centre for Neuromuscular Disease, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.
Steven Hillock
Bernard J Jasmin
University of Ottawa · CAUniversité Côte d'Azur · FR

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Disuse-induced skeletal muscle atrophy occurs following chronic periods of inactivity such as those involving prolonged bed rest, trauma and microgravity environments. Deconditioning of skeletal muscle is mainly characterized by a loss of muscle mass, decreased fibre cross-sectional area, reduced force, increased fatigability, increased insulin resistance and transitions in fibre types. A description of the role of specific transcriptional mechanisms contributing to muscle atrophy by altering gene expression during muscle disuse has recently emerged and focused primarily on short period of inactivity. A better understanding of the transduction pathways involved in activation of proteolytic and apoptotic pathways continues to represent a major objective, together with the study of potential cross-talks in these cellular events. In parallel, evaluation of the impact of countermeasures at the cellular and molecular levels in short- and long-term disuse experimentations or microgravity environments should undoubtedly and synergistically increase our basic knowledge in attempts to identify new physical, pharmacological and nutritional targets to counteract muscle atrophy. These investigations are important as skeletal muscle atrophy remains an important neuromuscular challenge with impact in clinical and social settings affecting a variety of conditions such as those seen in aging, cancer cachexia, muscle pathologies and long-term space exploration.

Indexed as

Gene Expression RegulationAnimalsApoptosisHumansIntercellular Signaling Peptides and ProteinsMiceMuscle, SkeletalMuscular AtrophyMuscular Disorders, AtrophicNF-kappa BProteasome Endopeptidase ComplexSignal TransductionWeightlessnessIntercellular Signaling Peptides and ProteinsNF-kappa BProteasome Endopeptidase Complex

Identifiers

PMID19656243
PMCPMC4516463
OpenAlexW2104654683

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.