Evidence map›Paper›PMID 27555760›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2016

Critical role of tumor necrosis factor receptor 1 in the pathogenesis of pulmonary emphysema in mice.

Masaki Fujita, Hiroshi Ouchi, Satoshi Ikegame, Eiji Harada, Takemasa Matsumoto, Junji Uchino, Yoichi Nakanishi, Kentaro Watanabe

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Roundabout signaling pathway involved in the pathogenesis of COPD by integrative bioinformatics analysis.International journal of chronic obstructive pulmonary disease · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. ChronicInternational journal of chronic obstructive pulmonary disease · 2016
    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

8 authors at 2 institutions in 1 country.

Masaki FujitaDepartment of Respiratory Medicine, Faculty of Medicine, Fukuoka University.
Hiroshi OuchiResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Satoshi IkegameResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Eiji HaradaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Takemasa MatsumotoDepartment of Respiratory Medicine, Faculty of Medicine, Fukuoka University.
Junji UchinoDepartment of Respiratory Medicine, Faculty of Medicine, Fukuoka University.
Yoichi NakanishiResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kentaro WatanabeDepartment of Respiratory Medicine, Faculty of Medicine, Fukuoka University.
Fukuoka University · JPKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COPD is a major cause of chronic morbidity and mortality throughout the world. Although tumor necrosis factor-α (TNF-α) has a critical role in the development of COPD, the role of different TNF receptors (TNFRs) in pulmonary emphysema has not been resolved. We aimed to clarify the role of TNFRs in the development of pulmonary emphysema. TNF-α transgenic mice, a murine model of COPD in which the mice spontaneously develop emphysema with a large increase in lung volume and pulmonary hypertension, were crossed with either TNFR1-deficient mice or TNFR2-deficient mice. After 6 months, the gross appearance of the lung, lung histology, and pulmonary and cardiac physiology were determined. In addition, the relationship between apoptosis and emphysema was investigated. Pulmonary emphysema-like changes disappeared with deletion of TNFR1. However, slight improvements were attained with deletion of TNFR2. Apoptotic cells in the interstitium of the lung were observed in TNF-α transgenic mice. The apoptotic signals through TNFR1 appear critical for the pathogenesis of pulmonary emphysema. In contrast, the inflammatory process has a less important role for the development of emphysema.

Indexed as

AnimalsApoptosisDisease Models, AnimalGenetic Predisposition to DiseaseLungMice, Inbred C57BLMice, KnockoutMice, TransgenicPhenotypePulmonary EmphysemaReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISignal TransductionTumor Necrosis Factor-alphaReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITnfrsf1a protein, mouseTumor Necrosis Factor-alphaapoptosisemphysemareceptorTNF-α

Identifiers

PMID27555760
PMCPMC4968668
OpenAlexW2488681476

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.