Evidence map›Paper›PMID 24669297›Full record

ReviewF1000prime reports2014

The treatment of idiopathic pulmonary fibrosis.

Hannah V Woodcock, Toby M Maher

Open access · bronzeAbstract readReview
In one paragraph

Review in F1000prime reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Review
  3. CRTH2 Mediates Profibrotic Macrophage Differentiation and Promotes Lung Fibrosis.American journal of respiratory cell and molecular biology · 2022
    Article
  4. Review
  5. Review
  6. TGF-β Promotes Metabolic Reprogramming in Lung Fibroblasts via mTORC1-dependent ATF4 Activation.American journal of respiratory cell and molecular biology · 2020
    Article
  7. Glutamine Metabolism Is Required for Collagen Protein Synthesis in Lung Fibroblasts.American journal of respiratory cell and molecular biology · 2019
    Article
  8. Effect of dermatan sulphate on a C57-mouse model of pulmonary fibrosis.The Journal of international medical research · 2019
    Article
  9. Article
  10. Article
  11. Inhibition of Phosphoglycerate Dehydrogenase Attenuates Bleomycin-induced Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Increased Cellular NADTuberculosis and respiratory diseases · 2016
    Article
  19. Lung Pericytes and Resident Fibroblasts: Busy Multitaskers.The American journal of pathology · 2016
    Review
  20. Precision medicine in idiopathic pulmonary fibrosis.QJM : monthly journal of the Association of Physicians · 2016
    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

2 authors at 2 institutions in 1 country.

Hannah V WoodcockNIHR Respiratory Biomedical Research Unit, Royal Brompton Hospital Sydney Street, London, SW3 6NP UK ; Centre for Inflammation and Tissue Repair, University College London, Rayne Institute 5 University Road, London, WC1E 6JJ UK.
Toby M MaherNIHR Respiratory Biomedical Research Unit, Royal Brompton Hospital Sydney Street, London, SW3 6NP UK ; Centre for Leucocyte Biology, Imperial College London Sir Alexander Fleming Building, London, SW3 UK.
NIHR Royal Brompton Cardiovascular Biomedical Research Unit · GBRoyal Brompton Hospital · GB

Funding

Medical Research Council MR/K024078/1
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive and invariably fatal disease with a median survival of less than three years from diagnosis. The last decade has seen an exponential increase in clinical trial activity in IPF and this in turn has led to important developments in the treatment of this terrible disease. Previous therapeutic approaches based around regimens including corticosteroids and azathioprine have, when tested in randomized clinical trials, been shown to be harmful in IPF. By contrast, compounds with anti-fibrotic actions have been shown to be beneficial. Subsequently, the novel anti-fibrotic agent pirfenidone has, in many parts of the world, become the first treatment ever to be licensed for use in IPF. This exciting development, coupled with ongoing clinical trials of a range of other novel compounds, is bringing hope to patients and their clinicians and raises the prospect that, in the future, it may become possible to successfully arrest the development of progressive scarring in IPF.

Identifiers

PMID24669297
PMCPMC3944742
OpenAlexW2004653413

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.