Evidence map›Paper›PMID 26209274›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015

NAD(P)H oxidase subunit p47phox is elevated, and p47phox knockout prevents diaphragm contractile dysfunction in heart failure.

Bumsoo Ahn, Adam W Beharry, Gregory S Frye, Andrew R Judge, Leonardo F Ferreira

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2015. 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
3.6field-weighted citation impact, top 6% 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, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Redox Control of Skeletal Muscle Function and Adaptations to Exercise.Advances in experimental medicine and biology · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Locomotor and respiratory muscle abnormalities in HFrEF and HFpEF.Frontiers in cardiovascular medicine · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mitochondrial respiration and HAmerican journal of physiology. Cell physiology · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Bumsoo AhnDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida; and.
Adam W BeharryDepartment of Physical Therapy, University of Florida, Gainesville, Florida.
Gregory S FryeDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida; and.
Andrew R JudgeDepartment of Physical Therapy, University of Florida, Gainesville, Florida.
Leonardo F FerreiraDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida; and Ferreira@hhp.ufl.edu.
University of Florida · US

Funding

FOXO signaling and skeletal muscle atrophyR01AR060209 · NIAMS · UNIVERSITY OF FLORIDA · PI JUDGE, ANDREW ROBERT · 2011 to 2021
$4.2M
Mechanisms of Respiratory Muscle Dysfunction in Heart FailureR00HL098453 · NHLBI · UNIVERSITY OF FLORIDA · PI FERREIRA, LEONARDO · 2011 to 2013
$735k
NHLBI NIH HHS R00 HL098453NHLBI NIH HHS R00-HL-098453NIAMS NIH HHS R01-AR-060209
6 · The paper itself

Abstract

Patients with chronic heart failure (CHF) have dyspnea and exercise intolerance, which are caused in part by diaphragm abnormalities. Oxidants impair diaphragm contractile function, and CHF increases diaphragm oxidants. However, the specific source of oxidants and its relevance to diaphragm abnormalities in CHF is unclear. The p47(phox)-dependent Nox2 isoform of NAD(P)H oxidase is a putative source of diaphragm oxidants. Thus, we conducted our study with the goal of determining the effects of CHF on the diaphragm levels of Nox2 complex subunits and test the hypothesis that p47(phox) knockout prevents diaphragm contractile dysfunction elicited by CHF. CHF caused a two- to sixfold increase (P < 0.05) in diaphragm mRNA and protein levels of several Nox2 subunits, with p47(phox) being upregulated and hyperphosphorylated. CHF increased diaphragm extracellular oxidant emission in wild-type but not p47(phox) knockout mice. Diaphragm isometric force, shortening velocity, and peak power were decreased by 20-50% in CHF wild-type mice (P < 0.05), whereas p47(phox) knockout mice were protected from impairments in diaphragm contractile function elicited by CHF. Our experiments show that p47(phox) is upregulated and involved in the increased oxidants and contractile dysfunction in CHF diaphragm. These findings suggest that a p47(phox)-dependent NAD(P)H oxidase mediates the increase in diaphragm oxidants and contractile dysfunction in CHF.

Indexed as

AnimalsCoronary VesselsDiaphragmDisease Models, AnimalEchocardiographyHeart FailureMaleMiceMice, Inbred C57BLMice, KnockoutMuscle ContractionMyocardial InfarctionNADPH OxidasesOxidation-ReductionOxidative StressPhosphorylationNADPH Oxidasesneutrophil cytosolic factor 1RNA, Messengermyocardial infarctionoxidative stressrespiratory muscle

Identifiers

PMID26209274
PMCPMC4556931
OpenAlexW2176125277

What OpenQuestion holds

Textmetadata
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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.