Evidence map›Paper›PMID 18218129›Full record

ArticleRespiratory research2008

Diaphragm adaptations in patients with COPD.

Coen A C Ottenheijm, Leo M A Heunks, Richard P N Dekhuijzen

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 6 pooled it
5.1field-weighted citation impact, top 5% 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

63 citing papers in PubMed, 6 syntheses or guidelines pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Respiratory Muscle Strength and Mortality in Patients with COPD: A Systematic Review and Meta-Analysis.International journal of chronic obstructive pulmonary disease · 2025
    Pooled it
  3. Pooled it
  4. Chronic non-invasive ventilation for chronic obstructive pulmonary disease.The Cochrane database of systematic reviews · 2021
    Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Article
  9. Review
  10. Article
  11. Article
  12. Observational
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Diaphragm and Lung Transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2024
    Review
  20. Article

3 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Coen A C OttenheijmDept. of Molecular and Cellular Biology, University of Arizona, Tucson, USA. coeno@email.arizona.edu
Leo M A Heunks
Richard P N Dekhuijzen
Radboud University Nijmegen · NLUniversity of Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inspiratory muscle weakness in patients with COPD is of major clinical relevance. For instance, maximum inspiratory pressure generation is an independent determinant of survival in severe COPD. Traditionally, inspiratory muscle weakness has been ascribed to hyperinflation-induced diaphragm shortening. However, more recently, invasive evaluation of diaphragm contractile function, structure, and biochemistry demonstrated that cellular and molecular alterations occur, of which several can be considered pathologic of nature. Whereas the fiber type shift towards oxidative type I fibers in COPD diaphragm is regarded beneficial, rendering the overloaded diaphragm more resistant to fatigue, the reduction of diaphragm fiber force generation in vitro likely contributes to diaphragm weakness. The reduced diaphragm force generation at single fiber level is associated with loss of myosin content in these fibers. Moreover, the diaphragm in COPD is exposed to oxidative stress and sarcomeric injury. This review postulates that the oxidative stress and sarcomeric injury activate proteolytic machinery, leading to contractile protein wasting and, consequently, loss of force generating capacity of diaphragm fibers in patients with COPD. Interestingly, several of these presumed pathologic alterations are already present early in the course of the disease (GOLD I/II), although these patients appear not limited in their daily life activities. Treatment of diaphragm dysfunction in COPD is complex since its etiology is unclear, but recent findings indicate the ubiquitin-proteasome pathway as a prime target to attenuate diaphragm wasting in COPD.

Indexed as

Models, BiologicalMuscle ContractionAdaptation, PhysiologicalAnimalsDiaphragmHumansMuscular AtrophyPulmonary Disease, Chronic Obstructive

Identifiers

PMID18218129
PMCPMC2248576
OpenAlexW2171177416

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.