Evidence map›Paper›PMID 27611888›Full record

ArticleRedox biology2016

Levels of inflammation and oxidative stress, and a role for taurine in dystropathology of the Golden Retriever Muscular Dystrophy dog model for Duchenne Muscular Dystrophy.

Jessica R Terrill, Marisa N Duong, Rufus Turner, Caroline Le Guiner, Amber Boyatzis, Anthony J Kettle, Miranda D Grounds, Peter G Arthur

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025
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  6. Caveolin and NOS in the Development of Muscular Dystrophy.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
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  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Description of Osmolyte Pathways in MaturingInternational journal of molecular sciences · 2022
    Article
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

8 authors at 3 institutions in 3 countries.

Jessica R TerrillSchool of Chemistry and Biochemistry, the University of Western Australia, Perth, Western Australia, Australia; School of Anatomy, Physiology and Human Biology, the University of Western Australia, Perth, Western Australia, Australia. Electronic address: jessica.terrill@uwa.edu.au.
Marisa N DuongSchool of Chemistry and Biochemistry, the University of Western Australia, Perth, Western Australia, Australia.
Rufus TurnerCentre for Free Radical Research, Department of Pathology, the University of Otago, Christchurch, New Zealand.
Caroline Le GuinerAtlantic Gene Therapies, INSERM UMR1089, Nantes, France; Genethon, Evry, France.
Amber BoyatzisSchool of Chemistry and Biochemistry, the University of Western Australia, Perth, Western Australia, Australia.
Anthony J KettleCentre for Free Radical Research, Department of Pathology, the University of Otago, Christchurch, New Zealand.
Miranda D GroundsSchool of Anatomy, Physiology and Human Biology, the University of Western Australia, Perth, Western Australia, Australia.
Peter G ArthurSchool of Chemistry and Biochemistry, the University of Western Australia, Perth, Western Australia, Australia.
University of Western Australia · AUUniversity of Otago · NZGenethon (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne Muscular Dystrophy (DMD) is a fatal skeletal muscle wasting disease presenting with excessive myofibre necrosis and increased inflammation and oxidative stress. In the mdx mouse model of DMD, homeostasis of the amino acid taurine is altered, and taurine administration drastically decreases muscle necrosis, dystropathology, inflammation and protein thiol oxidation. Since the severe pathology of the Golden Retriever Muscular Dystrophy (GRMD) dog model more closely resembles the human DMD condition, we aimed to assess the generation of oxidants by inflammatory cells and taurine metabolism in this species. In muscles of 8 month GRMD dogs there was an increase in the content of neutrophils and macrophages, and an associated increase in elevated myeloperoxidase, a protein secreted by neutrophils that catalyses production of the highly reactive hypochlorous acid (HOCl). There was also increased chlorination of tyrosines, a marker of HOCl generation, increased thiol oxidation of many proteins and irreversible oxidative protein damage. Taurine, which functions as an antioxidant by trapping HOCl, was reduced in GRMD plasma; however taurine was increased in GRMD muscle tissue, potentially due to increased muscle taurine transport and synthesis. These data indicate a role for HOCl generated by neutrophils in the severe dystropathology of GRMD dogs, which may be exacerbated by decreased availability of taurine in the blood. These novel data support continued research into the precise roles of oxidative stress and taurine in DMD and emphasise the value of the GRMD dogs as a suitable pre-clinical model for testing taurine as a therapeutic intervention for DMD boys.

Indexed as

Oxidative StressAnimalsBiomarkersDisease Models, AnimalDogsInflammationMacrophagesMaleMuscle ProteinsMuscle, SkeletalMuscular Dystrophy, DuchenneNeutrophilsOxidation-ReductionPeroxidaseTyrosineBiomarkersMuscle ProteinsPeroxidaseTyrosineDuchenne Muscular Dystrophy (DMD)Golden Retriever Muscular Dystrophy (GRMD)InflammationOxidative stressProtein thiol oxidationTaurine

Identifiers

PMID27611888
PMCPMC5018082
OpenAlexW2511362678

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.