Evidence map›Paper›PMID 11087833›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Functional muscle ischemia in neuronal nitric oxide synthase-deficient skeletal muscle of children with Duchenne muscular dystrophy.

M Sander, B Chavoshan, S A Harris, S T Iannaccone, J T Stull, G D Thomas, R G Victor

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 5 pooled it
7.1field-weighted citation impact, top 2% 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

188 citing papers in PubMed, 5 syntheses or guidelines pooled it, 439 citations in OpenAlex.

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  5. WHOLE-BODY VIBRATION EXERCISE IS WELL TOLERATED IN PATIENTS WITH DUCHENNE MUSCULAR DYSTROPHY: A SYSTEMATIC REVIEW.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2017
    Pooled it
  6. Inspiratory muscle training in children with neuromuscular disorders.The South African journal of physiotherapy · 2024
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  8. Effects of Sildenafil on Cerebrovascular Reactivity in Patients with Becker Muscular Dystrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
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128 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

M SanderCopenhagen Muscle Research Center, Rigshospitalet, DK-2200, Copenhagen N, Denmark.
B Chavoshan
S A Harris
S T Iannaccone
J T Stull
G D Thomas
R G Victor
Rigshospitalet · DKThe University of Texas Southwestern Medical Center · USSouthwestern Medical Center · US

Funding

Transcriptional control of muscle growth and remodelingP01HL006296 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA · 1985 to 2006
$14.8M
TRAINING IN CARDIOVASCULAR RESEARCHT32HL007360 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 1985 to 2012
$11.8M
NHLBI NIH HHS HL06296NHLBI NIH HHS HL07360NHLBI NIH HHS P01 HL006296NHLBI NIH HHS T32 HL007360
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a fatal disease caused by mutation of the gene encoding the cytoskeletal protein dystrophin. Despite a wealth of recent information about the molecular basis of DMD, effective treatment for this disease does not exist because the mechanism by which dystrophin deficiency produces the clinical phenotype is unknown. In both mouse and human skeletal muscle, dystrophin deficiency results in loss of neuronal nitric oxide synthase, which normally is localized to the sarcolemma as part of the dystrophin-glycoprotein complex. Recent studies in mice suggest that skeletal muscle-derived nitric oxide may play a key role in the regulation of blood flow within exercising skeletal muscle by blunting the vasoconstrictor response to alpha-adrenergic receptor activation. Here we report that this protective mechanism is defective in children with DMD, because the vasoconstrictor response (measured as a decrease in muscle oxygenation) to reflex sympathetic activation was not blunted during exercise of the dystrophic muscles. In contrast, this protective mechanism is intact in healthy children and those with polymyositis or limb-girdle muscular dystrophy, muscle diseases that do not result in loss of neuronal nitric oxide synthase. This clinical investigation suggests that unopposed sympathetic vasoconstriction in exercising human skeletal muscle may constitute a heretofore unappreciated vascular mechanism contributing to the pathogenesis of DMD.

Indexed as

AdolescentCase-Control StudiesChildFemaleHumansIschemiaMaleMuscle, SkeletalMuscular Dystrophy, DuchenneNitric Oxide SynthaseNitric Oxide Synthase Type INitric Oxide SynthaseNitric Oxide Synthase Type INOS1 protein, human

Identifiers

PMID11087833
PMCPMC17659
OpenAlexW2033676880

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.