Evidence map›Paper›PMID 23104273›Full record

ReviewJournal of muscle research and cell motility2013

Contribution of oxidative stress to pathology in diaphragm and limb muscles with Duchenne muscular dystrophy.

Jong-Hee Kim, Hyo-Bum Kwak, LaDora V Thompson, John M Lawler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of muscle research and cell motility, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Special Issue "Skeletal Muscle Adaptations to Oxidative Stress".International journal of molecular sciences · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Caveolin and NOS in the Development of Muscular Dystrophy.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. A fat- and sucrose-enriched diet causes metabolic alterations in mdx mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  13. Curcumin Administration Improves Force ofAntioxidants (Basel, Switzerland) · 2023
    Article
  14. Review
  15. Article
  16. Review
  17. BKPharmaceutics · 2022
    Article
  18. Article
  19. Review
  20. Effects of muscle damage onNMR in biomedicine · 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

4 authors at 3 institutions in 2 countries.

Jong-Hee KimDepartment of Physical Medicine and Rehabilitation, University of Minnesota Medical School, Minneapolis, 55455, USA. kimx2355@umn.edu
Hyo-Bum Kwak
LaDora V Thompson
John M Lawler
University of Minnesota Medical Center · USInha University · KRTexas A&M University · US

Funding

Structural and Calcium Regulatory Proteins in SarcopeniaR01AG017768 · NIA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI THOMPSON, LADORA V · 2001 to 2012
$3.0M
Regulation of Oxidative Stress in the mdx DiaphragmR03AR054084 · NIAMS · TEXAS A&M UNIVERSITY · PI LAWLER, JOHN M · 2006 to 2008
$204k
NIAMS NIH HHS AR054084NIA NIH HHS AG017768
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a degenerative skeletal muscle disease that makes walking and breathing difficult. DMD is caused by an X-linked (Xp21) mutation in the dystrophin gene. Dystrophin is a scaffolding protein located in the sarcolemmal cytoskeleton, important in maintaining structural integrity and regulating muscle cell (muscle fiber) growth and repair. Dystrophin deficiency in mouse models (e.g., mdx mouse) destabilizes the interface between muscle fibers and the extracellular matrix, resulting in profound damage, inflammation, and weakness in diaphragm and limb muscles. While the link between dystrophin deficiency with inflammation and pathology is multi-factorial, elevated oxidative stress has been proposed as a central mediator. Unfortunately, the use of non-specific antioxidant scavengers in mouse and human studies has led to inconsistent results, obscuring our understanding of the importance of redox signaling in pathology of muscular dystrophy. However, recent studies with more mechanistic approaches in mdx mice suggest that NAD(P)H oxidase and nuclear factor-kappaB are important in amplifying dystrophin-deficient muscle pathology. Therefore, more targeted antioxidant therapeutics may ameliorate damage and weakness in human population, thus promoting better muscle function and quality of life. This review will focus upon the pathobiology of dystrophin deficiency in diaphragm and limb muscle primarily in mouse models, with a rationale for development of targeted therapeutic antioxidants in DMD patients.

Indexed as

Oxidative StressAnimalsAntioxidantsClinical Trials as TopicDiaphragmDystrophinHumansInflammationMiceMice, Inbred mdxMusclesMuscular Dystrophy, DuchenneNADPH OxidasesNF-kappa BAntioxidantsDystrophinNADPH OxidasesNF-kappa B

Identifiers

PMID23104273
OpenAlexW2065717274

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.