Evidence map›Paper›PMID 14969575›Full record

ReviewDrugs2004

Idiopathic pulmonary fibrosis: pathogenesis and therapeutic approaches.

Moisés Selman, Victor J Thannickal, Annie Pardo, David A Zisman, Fernando J Martinez, Joseph P Lynch

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05353556 (Effects of Home-based Inspiratory Muscle Training in Patients With Idiopathic Pulmonary Fibrosis), which is not on this map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
21.6field-weighted citation impact, top 1% 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.

NCT05353556 nacompletednot on this mapstarted 2022, after this paper: background citation

Effects of Home-based Inspiratory Muscle Training in Patients With Idiopathic Pulmonary Fibrosis

TypeinterventionalSponsorDokuz Eylul UniversityRan2022 to 2022Enrolled28ConditionsIdiopathic Pulmonary Fibrosis, IPFArmsInspiratory Muscle Training (IMT), Sham IMT
3 · Its place in the literature

Who cites it

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. ASK1ng to Delay the Progression of Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Lipid Metabolism Profiles in Rheumatic Diseases.Frontiers in pharmacology · 2021
    Review
  19. Article
  20. Review

30 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

6 authors at 4 institutions in 2 countries.

Moisés SelmanInstituto Nacional de Enfermedades Respiratorias, Mexico DF, Mexico. mselman@sni.conacyt.mx
Victor J Thannickal
Annie Pardo
David A Zisman
Fernando J Martinez
Joseph P Lynch
University of California, Los Angeles · USUniversity of Michigan–Ann Arbor · USInstituto Nacional de Enfermedades Respiratorias · MXUniversidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF), also termed cryptogenic fibrosing alveolitis, is a clinicopathological syndrome characterised by cough, exertional dyspneoa, basilar crackles, a restrictive defect on pulmonary function tests, honeycombing on high-resolution, thin-section computed tomographic scans and the histological diagnosis of usual interstitial pneumonia on lung biopsy. The course is usually indolent but inexorable. Most patients die of progressive respiratory failure within 3-8 years of the onset of symptoms. Current therapies are of unproven benefit. Although the pathogenesis of IPF has not been elucidated, early concepts focused on lung injury leading to a cycle of chronic alveolar inflammation eventuating in fibrosis and destruction of the lung architecture. Anti-inflammatory therapies employing corticosteroids or immunosuppressive or cytotoxic agents have been disappointing. More recent hypotheses acknowledge that sequential alveolar epithelial cell injury is likely to be a key event in the pathogenesis of IPF, but the cardinal event is an aberrant host response to wound healing. In this context, abnormal epithelial-mesenchymal interactions, altered fibroblast phenotypes, exaggerated fibroblast proliferation, and excessive deposition of collagen and extracellular matrix are pivotal to the fibrotic process. Several clinical trials are currently underway or in the planning stages, and include drugs such as interferon-gamma 1b, pirfenidone, acetylcysteine, etanercept (a tumor necrosis factor-alpha antagonist), bosentan (an endothelin-1 receptor antagonist) and zileuton (a 5-lypoxygenase inhibitor). Future therapeutic strategies should be focused on alveolar epithelial cells aimed at enhancing re-epithelialisation and on fibroblastic/myofibroblastic foci, which play an essential role in the development of IPF. Stem cell progenitors of the alveolar epithelial cells and genetic and epigenetic therapies are attractive future approaches for this and other fibrotic lung disorders.

Indexed as

Clinical Trials as TopicGenetic TherapyHumansPulmonary Fibrosis

Identifiers

PMID14969575
OpenAlexW2022862004

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.