Evidence map›Paper›PMID 22443334›Full record

ArticleBMC musculoskeletal disorders2012

Calpain 3 is important for muscle regeneration: evidence from patients with limb girdle muscular dystrophies.

Simon Hauerslev, Marie-Louise Sveen, Morten Duno, Corrado Angelini, John Vissing, Thomas O Krag

Open access · goldAbstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

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  11. Compound heterozygousMolecular medicine reports · 2021
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  13. Rescue of Advanced Pompe Disease in Mice with Hepatic Expression of Secretable Acid α-Glucosidase.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  14. Gene Correction of LGMD2A Patient-Specific iPSCs for the Development of Targeted Autologous Cell Therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  15. Phenotypic and genetic spectrum of patients with limb-girdle muscular dystrophy type 2A from Serbia.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2019
    Article
  16. Analgesic Effects ofEvidence-based complementary and alternative medicine : eCAM · 2019
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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

6 authors at 2 institutions in 2 countries.

Simon HauerslevDepartment of Neurology, Neuromuscular Research Unit, The Copenhagen Muscle Research Center, Rigshospitalet, Blegdamsvej 9, Copenhagen, Denmark.
Marie-Louise Sveen
Morten Duno
Corrado Angelini
John Vissing
Thomas O Krag
Rigshospitalet · DKUniversity of Padua · IT

Funding

Telethon GTB07001
6 · The paper itself

Abstract

backgroundLimb girdle muscular dystrophy (LGMD) type 2A is caused by mutations in the CAPN3 gene and complete lack of functional calpain 3 leads to the most severe muscle wasting. Calpain 3 is suggested to be involved in maturation of contractile elements after muscle degeneration. The aim of this study was to investigate how mutations in the four functional domains of calpain 3 affect muscle regeneration.

methodsWe studied muscle regeneration in 22 patients with LGMD2A with calpain 3 deficiency, in five patients with LGMD2I, with a secondary reduction in calpain 3, and in five patients with Becker muscular dystrophy (BMD) with normal calpain 3 levels. Regeneration was assessed by using the developmental markers neonatal myosin heavy chain (nMHC), vimentin, MyoD and myogenin and counting internally nucleated fibers.

resultsWe found that the recent regeneration as determined by the number of nMHC/vimentin-positive fibers was greatly diminished in severely affected LGMD2A patients compared to similarly affected patients with LGMD2I and BMD. Whorled fibers, a sign of aberrant regeneration, was highly elevated in patients with a complete lack of calpain 3 compared to patients with residual calpain 3. Regeneration is not affected by location of the mutation in the CAPN3 gene.

conclusionsOur findings suggest that calpain 3 is needed for the regenerative process probably during sarcomere remodeling as the complete lack of functional calpain 3 leads to the most severe phenotypes.

Indexed as

RegenerationAdolescentAdultApoptosisBiomarkersBiopsyBlotting, WesternCalpainDenmarkDystrophinFemaleGenetic Predisposition to DiseaseHumansImmunohistochemistryLinear ModelsMaleBiomarkersCalpainCAPN3 protein, humanDystrophinFKRP protein, humanMuscle ProteinsMyoD1 myogenic differentiation proteinMyoD ProteinMyogeninMYOG protein, humanMyosin Heavy ChainsPentosyltransferasesProteinsVimentin

Identifiers

PMID22443334
PMCPMC3338386
OpenAlexW1991487249

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.