Evidence map›Paper›PMID 25740330›Full record

ReviewDisease models & mechanisms2015

Animal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapy.

Joe W McGreevy, Chady H Hakim, Mark A McIntosh, Dongsheng Duan

Open access · goldAbstract readReview
In one paragraph

Review in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 314 papers.

0numbers the graph read from it
0cells of the map it votes in
314citing papers in PubMed
19.9field-weighted citation impact, top 1% 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

314 citing papers in PubMed, 496 citations in OpenAlex.

  1. Article
  2. Ryanodine Receptor CaActa physiologica (Oxford, England) · 2026
    Article
  3. Article
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  5. AAVcc47-The Yale journal of biology and medicine · 2026
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  14. Review
  15. Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  16. Article
  17. Canine Model of Duchenne Muscular Dystrophy.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  18. Behavioral improvement in dystrophicMolecular therapy. Nucleic acids · 2025
    Article
  19. Article
  20. Article

254 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 1 institution in 1 country.

Joe W McGreevyDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212, USA.
Chady H HakimDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212, USA.
Mark A McIntoshDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212, USA.
Dongsheng DuanDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212, USA Department of Neurology, School of Medicine, University of Missouri, Columbia, MO 65212, USA duand@missouri.edu.
University of Missouri · US

Funding

Whole body single AAV microgene therapy in canine DMDR01NS090634 · NINDS · UNIVERSITY OF MISSOURI-COLUMBIA · PI Dongsheng Duan · 2015 to 2026
$4.2M
Dual AAV Vectors for Duchenne Muscular Dystrophy TherapyR01AR049419 · NIAMS · UNIVERSITY OF MISSOURI-COLUMBIA · PI DUAN, DONGSHENG · 2003 to 2012
$4.1M
Treatment of Duchenne Muscular Dystrophy with the Muscle Calcium PumpR01AR070517 · NIAMS · UNIVERSITY OF MISSOURI-COLUMBIA · PI DUAN, DONGSHENG · 2016 to 2020
$3.1M
Duchenne Cardiomyopathy Gene TherapyR01HL091883 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DUAN, DONGSHENG · 2010 to 2013
$2.0M
NHLBI NIH HHS HL-91883NHLBI NIH HHS R01 HL091883NIAMS NIH HHS AR-49419NIAMS NIH HHS R01 AR049419NIAMS NIH HHS R01 AR070517NINDS NIH HHS R01 NS090634
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a progressive muscle-wasting disorder. It is caused by loss-of-function mutations in the dystrophin gene. Currently, there is no cure. A highly promising therapeutic strategy is to replace or repair the defective dystrophin gene by gene therapy. Numerous animal models of DMD have been developed over the last 30 years, ranging from invertebrate to large mammalian models. mdx mice are the most commonly employed models in DMD research and have been used to lay the groundwork for DMD gene therapy. After ~30 years of development, the field has reached the stage at which the results in mdx mice can be validated and scaled-up in symptomatic large animals. The canine DMD (cDMD) model will be excellent for these studies. In this article, we review the animal models for DMD, the pros and cons of each model system, and the history and progress of preclinical DMD gene therapy research in the animal models. We also discuss the current and emerging challenges in this field and ways to address these challenges using animal models, in particular cDMD dogs.

Indexed as

Disease Models, AnimalGenetic TherapyAnimalsCardiomyopathiesDystrophinMuscular Dystrophy, DuchenneNeuronsDystrophinAnimal modelCanine DMDDuchenne muscular dystrophyDystrophinGene therapy

Identifiers

PMID25740330
PMCPMC4348559
OpenAlexW2097136884

What OpenQuestion holds

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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.