Evidence map›Paper›PMID 27924830›Full record

ArticleScientific reports2016

Impaired regenerative capacity and lower revertant fibre expansion in dystrophin-deficient mdx muscles on DBA/2 background.

Merryl Rodrigues, Yusuke Echigoya, Rika Maruyama, Kenji Rowel Q Lim, So-Ichiro Fukada, Toshifumi Yokota

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. The D2.B10-DmdThe American journal of pathology · 2026
    Article
  5. Skeletal muscle: a biologists' adventure playground.Journal of muscle research and cell motility · 2025
    Review
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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.

Merryl RodriguesDepartment of Medical Genetics, University of Alberta Faculty of Medicine and Dentistry, Edmonton, Alberta, T6G2H7, Canada.
Yusuke EchigoyaDepartment of Medical Genetics, University of Alberta Faculty of Medicine and Dentistry, Edmonton, Alberta, T6G2H7, Canada.
Rika MaruyamaDepartment of Medical Genetics, University of Alberta Faculty of Medicine and Dentistry, Edmonton, Alberta, T6G2H7, Canada.
Kenji Rowel Q LimDepartment of Medical Genetics, University of Alberta Faculty of Medicine and Dentistry, Edmonton, Alberta, T6G2H7, Canada.
So-Ichiro FukadaLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, 565-0871, Japan.
Toshifumi YokotaDepartment of Medical Genetics, University of Alberta Faculty of Medicine and Dentistry, Edmonton, Alberta, T6G2H7, Canada.

Funding

CIHR
6 · The paper itself

Abstract

Duchenne muscular dystrophy, one of the most common lethal genetic disorders, is caused by mutations in the DMD gene and a lack of dystrophin protein. In most DMD patients and animal models, sporadic dystrophin-positive muscle fibres, called revertant fibres (RFs), are observed in otherwise dystrophin-negative backgrounds. RFs are thought to arise from skeletal muscle precursor cells and clonally expand with age due to the frequent regeneration of necrotic fibres. Here we examined the effects of genetic background on muscle regeneration and RF expansion by comparing dystrophin-deficient mdx mice on the C57BL/6 background (mdx-B6) with those on the DBA/2 background (mdx-DBA), which have a more severe phenotype. Interestingly, mdx-DBA muscles had significantly lower RF expansion than mdx-B6 in all age groups, including 2, 6, 12, and 18 months. The percentage of centrally nucleated fibres was also significantly lower in mdx-DBA mice compared to mdx-B6, indicating that less muscle regeneration occurs in mdx-DBA. Our study aligns with the model that RF expansion reflects the activity of precursor cells in skeletal muscles, and it serves as an index of muscle regeneration capacity.

Indexed as

Genetic BackgroundAgingAnimalsCell ProliferationDisease Models, AnimalDystrophinFemaleGene ExpressionMaleMiceMice, Inbred C57BLMice, Inbred DBAMice, Inbred mdxMuscle Fibers, SkeletalMuscular Dystrophy, DuchenneMutationapo-dystrophin 1Dystrophin

Identifiers

PMID27924830
PMCPMC5141435

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Registered trials

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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.