Evidence map›Paper›PMID 14609023›Full record

ReviewJournal of muscle research and cell motility2003

Gene expression in muscle in response to exercise.

Geoffrey Goldspink

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of muscle research and cell motility, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Biophysics of ACL Injuries.Orthopedic reviews · 2024
    Article
  6. Review
  7. Review
  8. Review
  9. Low-frequency stimulation regulates metabolic gene expression in paralyzed muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2015
    Article
  10. Gene therapy for inherited muscle diseases: where genetics meets rehabilitation medicine.American journal of physical medicine & rehabilitation · 2014
    Review
  11. Article
  12. Are human and mouse satellite cells really the same?The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010
    Review
  13. Article
  14. Review
  15. Pax7 reveals a greater frequency and concentration of satellite cells at the ends of growing skeletal muscle fibers.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2008
    Article
  16. Tissue engineering in head and neck reconstructive surgery: what type of tissue do we need?European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2007
    Review
  17. Article
  18. Skeletal muscle tissue engineering.Journal of cellular and molecular medicine
    Review
  19. 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

1 author at 1 institution in 1 country.

Geoffrey GoldspinkMolecular Tissue Repair Unit, Department of Surgery, Royal Free and University College Medical School, Royal Free Campus, University of London, Rowland Hill Street, London NW3 2PF, UK. g.goldspink@rfc.ucl.ac.uk
University College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle has an intrinsic ability to adapt to different types of work by changing fibre type and muscle mass. This process involves quantitative and qualitative changes in gene expression including those of the myosin heavy chain (MyHC) isogenes that encode different types of molecular motors. Increased expression of slow MyHC and of metabolic genes result in increased fatigue resistance. Recently, there has been some insight into how oxidative metabolism, as well as slow myosin expression, is regulated and the role of calcium in initiating switches in gene expression. In relation to muscle mass and power output it has been appreciated that local as well as systemic factors are important. Our group have cloned three types of IGF-I in human muscle which are derived from the IGF-I gene by alternative splicing. The expression of one of these that appears to be an autocrine/paracrine splice variant is only detectable after mechanical stimulation (MGF) and a systemic type (IGF-IEa) that is produced by the liver and other tissue including muscle. As the result of a reading frame shift, the MGF peptide has a different C terminal sequence to IGF-IEa. Interestingly, the MGF C terminal peptide has been found to act as a separate growth factor and to initially activate mononluceated myoblasts (satellite cells). MGF also responds to different signals and has different expression kinetics to IGF-IEa. The mechanotransduction mechanism for this signalling may directly or indirectly involve the dystrophin complex as dystrophic muscle, unlike normal muscle, is unable to express MGF in response to overload. Also the ability to express MGF has been found to decline markedly during ageing. The deficiency in expressing MGF and activating satellite cells in dystrophic and aged muscles may explain why muscle mass is not maintained in these situations. However, in normal muscle MGF appears to initiate local muscle repair with its over expression resulting in hypertrophy.

Indexed as

Gene Expression ProfilingAnimalsCalciumExerciseGene Expression RegulationHumansInsulin-Like Growth Factor IMuscle Fibers, Fast-TwitchMuscle Fibers, SkeletalMuscle ProteinsMusclesMyosin Heavy ChainsPhenotypeCalciumInsulin-Like Growth Factor IMuscle ProteinsMyosin Heavy Chains

Identifiers

PMID14609023
OpenAlexW1583812535

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.