Evidence map›Paper›PMID 23558387›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2013

TNF signals via neuronal-type nitric oxide synthase and reactive oxygen species to depress specific force of skeletal muscle.

Shawn A Stasko, Brian J Hardin, Jeffrey D Smith, Jennifer S Moylan, Michael B Reid

Open access · greenAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Molecular mechanisms of postintensive care syndrome.Intensive care medicine experimental · 2021
    Review
  8. Skeletal muscle redox signaling in rheumatoid arthritis.Clinical science (London, England : 1979) · 2020
    Review
  9. Malondialdehyde as a Useful Biomarker of Low Hand Grip Strength in Community-Dwelling Stroke Patients.International journal of environmental research and public health · 2020
    Article
  10. Article
  11. Article
  12. Taurine transporter (TauT) deficiency impairs ammonia detoxification in mouse liver.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Article
  14. Review
  15. Protective Role of Eosinophils and TNFa after Ozone Inhalation.Research report (Health Effects Institute) · 2017
    Article
  16. Review
  17. Article
  18. Disease-Induced Skeletal Muscle Atrophy and Fatigue.Medicine and science in sports and exercise · 2016
    Review
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

Shawn A StaskoDepartment of Physiology and Center for Muscle Biology, University of Kentucky, Lexington, Kentucky 40356-0298, USA.
Brian J Hardin
Jeffrey D Smith
Jennifer S Moylan
Michael B Reid
University of Kentucky · US

Funding

Respiratory Muscle Weakness in Chronic InflammationR01AR055974 · NIAMS · UNIVERSITY OF KENTUCKY · PI ANDRADE, FRANCISCO H · 2009 to 2013
$1.6M
Research Training in Muscle Biology of Cardiopulmonary DiseaseT32HL086341 · NHLBI · UNIVERSITY OF KENTUCKY · PI ANDRADE, FRANCISCO H · 2008 to 2012
$610k
NHLBI NIH HHS 5 T32 HL086341-4NHLBI NIH HHS T32 HL086341NIAMS NIH HHS 5 R01-AR055974-04
6 · The paper itself

Abstract

TNF promotes skeletal muscle weakness, in part, by depressing specific force of muscle fibers. This is a rapid, receptor-mediated response, in which TNF stimulates cellular oxidant production, causing myofilament dysfunction. The oxidants appear to include nitric oxide (NO); otherwise, the redox mechanisms that underlie this response remain undefined. The current study tested the hypotheses that 1) TNF signals via neuronal-type NO synthase (nNOS) to depress specific force, and 2) muscle-derived reactive oxygen species (ROS) are essential co-mediators of this response. Mouse diaphragm fiber bundles were studied using live cell assays. TNF exposure increased general oxidant activity (P < 0.05; 2',7'-dichlorodihydrofluorescein diacetate assay) and NO activity (P < 0.05; 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate assay) and depressed specific force across the full range of stimulus frequencies (1-300 Hz; P < 0.05). These responses were abolished by pretreatment with N(ω)-nitro-L-arginine methyl ester (L-NAME; a nonspecific inhibitor of NOS activity), confirming NO involvement. Genetic nNOS deficiency replicated L-NAME effects on TNF-treated muscle, diminishing NO activity (-80%; P < 0.05) and preventing the decrement in specific force (P < 0.05). Comparable protection was achieved by selective depletion of muscle-derived ROS. Pretreatment with either SOD (degrades superoxide anion) or catalase (degrades hydrogen peroxide) depressed oxidant activity in TNF-treated muscle and abolished the decrement in specific force. These findings indicate that TNF signals via nNOS to depress contractile function, a response that requires ROS and NO as obligate co-mediators.

Indexed as

AnimalsCells, CulturedDiaphragmMaleMiceMice, Inbred C57BLMice, KnockoutMuscle StrengthNitric OxideNitric Oxide Synthase Type IReactive Oxygen SpeciesSignal TransductionTumor Necrosis Factor-alphaNitric OxideNitric Oxide Synthase Type INos1 protein, mouseReactive Oxygen SpeciesTumor Necrosis Factor-alphacytokinesdiaphragminflammationoxidative stressweakness

Identifiers

PMID23558387
PMCPMC3680824
OpenAlexW2059578219

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.