Evidence map›Paper›PMID 23185011›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Wnt7a treatment ameliorates muscular dystrophy.

Julia von Maltzahn, Jean-Marc Renaud, Gianni Parise, Michael A Rudnicki

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 124 citations in OpenAlex.

  1. Trial
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  6. Cellular and molecular bioengineering · 2025
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  12. Wnt7a is Required for Regeneration of Dystrophic Skeletal Muscle.bioRxiv : the preprint server for biology · 2024
    Article
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  16. Oligodendrocyte precursor cell transplantation promotes angiogenesis and remyelination via Wnt/Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Article
  17. Article
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  20. Review

10 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

4 authors at 4 institutions in 1 country.

Julia von MaltzahnSprott Center for Stem Cell Research, Ottawa Hospital Research Institute, Ottawa, ON, Canada K1H 8L6.
Jean-Marc Renaud
Gianni Parise
Michael A Rudnicki
McMaster University · CAOttawa Hospital · CAOttawa Hospital Research InstituteUniversity of Ottawa · CA

Funding

GENETIC REGULATION OF SKELETAL MUSCLE REPAIRR01AR044031 · NIAMS · OTTAWA HOSPITAL RESEARCH INSTITUTE · PI RUDNICKI, MICHAEL A · 1996 to 2025
$5.6M
Canadian Institutes of Health ResearchHoward Hughes Medical Institute
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a devastating genetic muscular disorder of childhood marked by progressive debilitating muscle weakness and wasting, and ultimately death in the second or third decade of life. Wnt7a signaling through its receptor Fzd7 accelerates and augments regeneration by stimulating satellite stem cell expansion through the planar cell polarity pathway, as well as myofiber hypertrophy through the AKT/mammalian target of rapamycin (mTOR) anabolic pathway. We investigated the therapeutic potential of the secreted factor Wnt7a for focal treatment of dystrophic DMD muscles using the mdx mouse model, and found that Wnt7a treatment efficiently induced satellite cell expansion and myofiber hypertrophy in treated mucles in mdx mice. Importantly, Wnt7a treatment resulted in a significant increase in muscle strength, as determined by generation of specific force. Furthermore, Wnt7a reduced the level of contractile damage, likely by inducing a shift in fiber type toward slow-twitch. Finally, we found that Wnt7a similarly induced myotube hypertrophy and a shift in fiber type toward slow-twitch in human primary myotubes. Taken together, our findings suggest that Wnt7a is a promising candidate for development as an ameliorative treatment for DMD.

Indexed as

AnimalsElectrochemotherapyGene Knockdown TechniquesGenetic TherapyHumansMaleMEF2 Transcription FactorsMiceMice, Inbred C57BLMice, Inbred mdxMuscle ContractionMuscle, SkeletalMuscular Dystrophy, AnimalMyogenic Regulatory FactorsPlasmidsRegenerationMef2c protein, mouseMEF2 Transcription FactorsMyogenic Regulatory FactorsRNA, MessengerWnt7a protein, mouseWnt Proteins

Identifiers

PMID23185011
PMCPMC3528612
OpenAlexW2013060005

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.