Evidence map›Paper›PMID 36359778›Full record

ArticleCells2022

A New Model of Acute Exacerbation of Experimental Pulmonary Fibrosis in Mice.

Céline-Hivda Yegen, Liasmine Haine, Kevin Da Costa Ferreira, Dominique Marchant, Jean-Francois Bernaudin, Carole Planès, Nicolas Voituron, Emilie Boncoeur

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Imaging technologies in experimental pulmonary fibrosis research: essential tool for enhanced translational relevance.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  5. Article
  6. Insights into interstitial lung disease pathogenesis.Breathe (Sheffield, England) · 2025
    Review
  7. Review
  8. Article
  9. Frontiers in medicine · 2024
    Article
  10. Review
  11. 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 1 institution in 1 country.

Céline-Hivda YegenLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.
Liasmine HaineLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.
Kevin Da Costa FerreiraLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.
Dominique MarchantLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.
Jean-Francois BernaudinLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.
Carole PlanèsLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.
Nicolas VoituronLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.ORCID 0000-0002-2092-4900
Emilie BoncoeurLaboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris-Nord, 93000 Bobigny, France.ORCID 0000-0002-1719-9808
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleidiopathic pulmonary fibrosis (IPF) is the most severe form of fibrosing interstitial lung disease, characterized by progressive respiratory failure leading to death. IPF's natural history is heterogeneous, and its progression unpredictable. Most patients develop a progressive decline of respiratory function over years; some remain stable, but others present a fast-respiratory deterioration without identifiable cause, classified as acute exacerbation (AE).

objectivesto develop and characterize an experimental mice model of lung fibrosis AE, mimicking IPF-AE at the functional, histopathological, cellular and molecular levels.

methodswe established in C57BL/6 male mice a chronic pulmonary fibrosis using a repetitive low-dose bleomycin (BLM) intratracheal (IT) instillation regimen (four instillations of BLM every 2 weeks), followed by two IT instillations of a simple or double-dose BLM challenge to induce AE. Clinical follow-up and histological and molecular analyses were done for fibrotic and inflammatory lung remodeling analysis. MEASUREMENTS AND MAIN

resultsas compared with a low-dose BLM regimen, this AE model induced a late burst of animal mortality, worsened lung fibrosis and remodeling, and superadded histopathological features as observed in humans IPF-AE. This was associated with stronger inflammation, increased macrophage infiltration of lung tissue and increased levels of pro-inflammatory cytokines in lung homogenates. Finally, it induced in the remodeled lung a diffuse expression of hypoxia-inducible factor 1α, a hallmark of tissular hypoxia response and a major player in the progression of IPF.

conclusionthis new model is a promising model of AE in chronic pulmonary fibrosis that could be relevant to mimic IPF-AE in preclinical trials.

Indexed as

Idiopathic Pulmonary FibrosisAnimalsBleomycinHumansHypoxiaLungMaleMiceMice, Inbred C57BLBleomycinacute exacerbationanimal modelinflammationlung fibrosis

Identifiers

PMID36359778
PMCPMC9654438
OpenAlexW4307303306

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.