Evidence map›Paper›PMID 28074267›Full record

ArticleJournal of neurology2017

Reduced serum myostatin concentrations associated with genetic muscle disease progression.

Peter M Burch, Oksana Pogoryelova, Joe Palandra, Richard Goldstein, Donald Bennett, Lori Fitz, Michela Guglieri, Chiara Marini Bettolo, Volker Straub, Teresinha Evangelista and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Observational
  4. Review
  5. Review
  6. Myostatin inhibition with orally administeredFrontiers in neurology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. A genetic model forOpen biology · 2022
    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

13 authors at 2 institutions in 2 countries.

Peter M BurchWorldwide Research and Development, Pfizer Inc., Eastern Point Road, Groton, CT, 06340, USA. peter.m.burch2@gmail.com.
Oksana PogoryelovaJohn Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Joe PalandraWorldwide Research and Development, Pfizer Inc., 1 Burtt Rd, Andover, MA, USA.
Richard GoldsteinWorldwide Research and Development, Pfizer Inc., Eastern Point Road, Groton, CT, 06340, USA.
Donald BennettWorldwide Research and Development, Pfizer Inc., 610 Main St., Cambridge, MA, USA.
Lori FitzWorldwide Research and Development, Pfizer Inc., 610 Main St., Cambridge, MA, USA.
Michela GuglieriJohn Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Chiara Marini BettoloJohn Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Volker StraubJohn Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Teresinha EvangelistaJohn Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Hendrik NeubertWorldwide Research and Development, Pfizer Inc., 1 Burtt Rd, Andover, MA, USA.
Hanns LochmüllerJohn Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Carl MorrisWorldwide Research and Development, Pfizer Inc., 610 Main St., Cambridge, MA, USA.
Pfizer (United States) · USNewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myostatin is a highly conserved protein secreted primarily from skeletal muscle that can potently suppress muscle growth. This ability to regulate skeletal muscle mass has sparked intense interest in the development of anti-myostatin therapies for a wide array of muscle disorders including sarcopenia, cachexia and genetic neuromuscular diseases. While a number of studies have examined the circulating myostatin concentrations in healthy and sarcopenic populations, very little data are available from inherited muscle disease patients. Here, we have measured the myostatin concentration in serum from seven genetic neuromuscular disorder patient populations using immunoaffinity LC-MS/MS. Average serum concentrations of myostatin in all seven muscle disease patient groups were significantly less than those measured in healthy controls. Furthermore, circulating myostatin concentrations correlated with clinical measures of disease progression for five of the muscle disease patient populations. These findings greatly expand the understanding of myostatin in neuromuscular disease and suggest its potential utility as a biomarker of disease progression.

Indexed as

AdolescentAdultAgedAged, 80 and overAnimalsBiomarkersBlood Chemical AnalysisChildChild, PreschoolCohort StudiesDisease ProgressionFemaleHumansMaleMice, Inbred C57BLMice, TransgenicBiomarkersMSTN protein, humanMyostatinBiomarkerMass spectrometryMyostatinNeuromuscular disease

Identifiers

PMID28074267
OpenAlexW2569924285

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.