Evidence map›Paper›PMID 22463481›Full record

ArticleJournal of anatomy2012

Characterisation of connective tissue from the hypertrophic skeletal muscle of myostatin null mice.

Mohamed I Elashry, Henry Collins-Hooper, Sakthivel Vaiyapuri, Ketan Patel

Open access · greenAbstract read
In one paragraph

Article in Journal of anatomy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

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  10. Myostatin deficiency partially rescues the bone phenotype of osteogenesis imperfecta model mice.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016
    Article
  11. 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

4 authors at 1 institution in 1 country.

Mohamed I ElashrySchool of Biological Sciences, University of Reading, Reading, UK.
Henry Collins-Hooper
Sakthivel Vaiyapuri
Ketan Patel
University of Reading · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myostatin is a potent inhibitor of muscle development. Genetic deletion of myostatin in mice results in muscle mass increase, with muscles often weighing three times their normal values. Contracting muscle transfers tension to skeletal elements through an elaborate connective tissue network. Therefore, the connective tissue of skeletal muscle is an integral component of the contractile apparatus. Here we examine the connective tissue architecture in myostatin null muscle. We show that the hypertrophic muscle has decreased connective tissue content compared with wild-type muscle. Secondly, we show that the hypertrophic muscle fails to show the normal increase in muscle connective tissue content during ageing. Therefore, genetic deletion of myostatin results in an increase in contractile elements but a decrease in connective tissue content. We propose a model based on the contractile profile of muscle fibres that reconciles this apparent incompatible tissue composition phenotype.

Indexed as

Analysis of VarianceAnimalsBlotting, WesternCollagenConnective TissueHypertrophyImmunohistochemistryMiceMice, KnockoutMicroscopy, Electron, ScanningModels, BiologicalMuscle ContractionMuscle, SkeletalMyostatinCollagenMyostatin

Identifiers

PMID22463481
PMCPMC3390513
OpenAlexW1801917292

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.