Evidence map›Paper›PMID 16003464›Full record

ArticleJournal of muscle research and cell motility2005

Effects of the compact mutant myostatin allele Mstn (Cmpt-dl1Abc) introgressed into a high growth mouse line on skeletal muscle cellularity.

Charlotte Rehfeldt, Gerhard Ott, David E Gerrard, László Varga, Werner Schlote, John L Williams, Ulla Renne, Lutz Bünger

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of muscle research and cell motility, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Polymorphism of Genes and Their Impact on Beef Quality.Current issues in molecular biology · 2023
    Review
  6. Combinatorial Inhibition of Myostatin and Activin A Improves Femoral Bone Properties in the G610C Mouse Model of Osteogenesis Imperfecta.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  7. Article
  8. Article
  9. Role of IGF-I in follistatin-induced skeletal muscle hypertrophy.American journal of physiology. Endocrinology and metabolism · 2015
    Article
  10. Article
  11. Review
  12. The compact mutation of myostatin causes a glycolytic shift in the phenotype of fast skeletal muscles.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Lack of myostatin results in excessive muscle growth but impaired force generation.Proceedings of the National Academy of Sciences of the United States of America · 2007
    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

8 authors at 7 institutions in 4 countries.

Charlotte RehfeldtDepartment of Muscle Biology and Growth, Research Institute for the Biology of Farm Animals, Wilhelm-Stahl-Allee 2, D-18196 Dummerstorf, Germany. rehfeldt@fbn-dummerstorf.de
Gerhard Ott
David E Gerrard
László Varga
Werner Schlote
John L Williams
Ulla Renne
Lutz Bünger
Research Institute for Farm Animal Biology (FBN) · DEAgricultural Biotechnology Institute · HUHumboldt-Universität zu Berlin · DEOstwestfalen-Lippe University of Applied Sciences and Arts · DEPurdue University West Lafayette · USRoslin Institute · GBUniversity of Edinburgh · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The murine myostatin mutation Mstn(Cmpt-dl1Abc) (Compact; C) was introduced into an inbred mouse line with extreme growth (DUHi) by marker-assisted introgression. To study the allelic effects on muscle fibre hyperplasia and hypertrophy, myonuclear proliferation, protein accretion, capillary density, and muscle fibre metabolism, samples from M. rectus femoris (RF) and M. longissimus dorsi (LD) muscles of animals wild-type (+/+), heterozygous (C/+), and homozygous (C/C) for the Mstn(Cmpt-dl1Abc) allele were examined by histological and biochemical analyses. Homozygous C/C mice exhibited lower body (-12%) but higher muscle weights (+38%) than ++ mice. Total muscle fibre number was increased (+24%), whereas fibre size was not significantly affected. Protein and DNA concentrations and DNA:protein ratios as well as specific CK activity remained unchanged for higher mass muscle implying increases in the total contents of DNA and muscle specific protein. Fibre type distribution was markedly shifted to the white glycolytic muscle fibres (+16-17% units) at the expense of red oxidative fibres. Capillary density was substantially lower in C/C than in ++ mice as seen by lower number of capillaries per fibre (-35%) and larger fibre area per capillary (+77%). However, the Mstn(Cmpt-dl1Abc) allele was partially recessive in heterozygous C/+ mice for both fibre type frequencies and capillary density. The results show that hypermuscularity caused by mutations in the myostatin gene results from muscle fibre hyperplasia rather than hypertrophy, and from balanced increases in myonuclear proliferation and protein accretion. However, capillary supply is adversely affected and muscle metabolism shifted towards glycolysis, which could have negative consequences for physical fitness.

Indexed as

AllelesAnimalsBody CompositionBody Weights and MeasuresCapillariesCrosses, GeneticFemaleHyperplasiaHypertrophyIn Vitro TechniquesMaleMiceMice, TransgenicMuscle Fibers, SkeletalMuscle, SkeletalMutationMstn protein, mouseMyostatinTransforming Growth Factor beta

Identifiers

PMID16003464
OpenAlexW2002216681

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.