Evidence map›Paper›PMID 24298022›Full record

ArticleMolecular and cellular biology2014

An antibody blocking activin type II receptors induces strong skeletal muscle hypertrophy and protects from atrophy.

Estelle Lach-Trifilieff, Giulia C Minetti, KellyAnn Sheppard, Chikwendu Ibebunjo, Jerome N Feige, Steffen Hartmann, Sophie Brachat, Helene Rivet, Claudia Koelbing, Frederic Morvan and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 4 pooled it
10.3field-weighted citation impact, top 1% 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

156 citing papers in PubMed, 4 syntheses or guidelines pooled it, 293 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Trial
  13. Trial
  14. Trial
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

96 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 2 countries.

Estelle Lach-TrifilieffMusculoSkeletal Diseases, Novartis Institutes for Biomedical Research, Basel, Switzerland.
Giulia C Minetti
KellyAnn Sheppard
Chikwendu Ibebunjo
Jerome N Feige
Steffen Hartmann
Sophie Brachat
Helene Rivet
Claudia Koelbing
Frederic Morvan
Shinji Hatakeyama
David J Glass
Novartis (Switzerland) · CHNovartis Institutes for BioMedical ResearchNovartis (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The myostatin/activin type II receptor (ActRII) pathway has been identified to be critical in regulating skeletal muscle size. Several other ligands, including GDF11 and the activins, signal through this pathway, suggesting that the ActRII receptors are major regulatory nodes in the regulation of muscle mass. We have developed a novel, human anti-ActRII antibody (bimagrumab, or BYM338) to prevent binding of ligands to the receptors and thus inhibit downstream signaling. BYM338 enhances differentiation of primary human skeletal myoblasts and counteracts the inhibition of differentiation induced by myostatin or activin A. BYM338 prevents myostatin- or activin A-induced atrophy through inhibition of Smad2/3 phosphorylation, thus sparing the myosin heavy chain from degradation. BYM338 dramatically increases skeletal muscle mass in mice, beyond sole inhibition of myostatin, detected by comparing the antibody with a myostatin inhibitor. A mouse version of the antibody induces enhanced muscle hypertrophy in myostatin mutant mice, further confirming a beneficial effect on muscle growth beyond myostatin inhibition alone through blockade of ActRII ligands. BYM338 protects muscles from glucocorticoid-induced atrophy and weakness via prevention of muscle and tetanic force losses. These data highlight the compelling therapeutic potential of BYM338 for the treatment of skeletal muscle atrophy and weakness in multiple settings.

Indexed as

Activin Receptors, Type IIActivinsAnimalsAntibodies, BlockingAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAtrophyCell DifferentiationHumansHypertrophyMiceMuscle, SkeletalMyoblasts, SkeletalSignal TransductionSmad2 ProteinSmad3 Proteinactivin AActivin Receptors, Type IIActivinsAntibodies, BlockingAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedbimagrumabSmad2 ProteinSmad3 Protein

Identifiers

PMID24298022
PMCPMC3911487
OpenAlexW2102107385

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.