Evidence map›Paper›PMID 25767391›Full record

ReviewTherapeutics and clinical risk management2015

Update on therapeutic management of idiopathic pulmonary fibrosis.

Argyris Tzouvelekis, Francesco Bonella, Paolo Spagnolo

Open access · goldAbstract readReview
In one paragraph

Review in Therapeutics and clinical risk management, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 4 pooled it
9.8field-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.

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

34 citing papers in PubMed, 4 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  13. Inhibition of the stem cell factor 248 isoform attenuates the development of pulmonary remodeling disease.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  14. Tackling MARCKS-PIP3 circuit attenuates fibroblast activation and fibrosis progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  15. Article
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  18. Article
  19. Effect of pirfenidone on wound healing in lung transplant patients.Multidisciplinary respiratory medicine · 2018
    Article
  20. 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

3 authors at 3 institutions in 3 countries.

Argyris TzouvelekisDepartment of Internal Medicine, Section of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, CT, USA.
Francesco BonellaInterstitial and Rare Lung Disease Unit, Ruhrlandklinik, University Hospital, University of Duisburg-Essen, Germany.
Paolo SpagnoloMedical University Clinic, Canton Hospital Baselland and University of Basel, Liestal, Switzerland.
Ruhrlandklinik · DEUniversity of Basel · CHYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive diffuse parenchymal lung disease of unknown origin, with a mortality rate exceeding that of many cancers. The diagnostic process is complex and relies on the clinician integrating clinical, laboratory, radiological, and histological data. In the last decade, major advances in our understanding of the pathogenesis of IPF have shifted the paradigm from a primarily inflammatory process evolving to fibrosis to a condition driven by aberrant wound healing following alveolar epithelial cell injury that results in scarring of the lung, architectural distortion, and irreversible loss of function. Improved understanding of disease pathogenesis has led to the identification of several therapeutic targets and the design of high-quality clinical trials evaluating novel compounds. However, the results of these studies have been mostly disappointing, probably due to the plethora of mediators, growth factors, and signaling pathways involved in the fibrotic process. Most recently, pirfenidone and nintedanib, two compounds with pleiotropic anti-fibrotic properties, have been proven effective in reducing functional decline and disease progression in IPF. This is a major breakthrough. Nevertheless, we still have a long way to go. In fact, neither pirfenidone nor nintedanib is a cure for IPF, and most patients continue to progress despite treatment. As such, comprehensive care of patients with IPF, including management of concomitant conditions and physical debility, as well as timely referral for lung transplantation, remains essential. Several agents with a high potential are currently being tested, and many more are ready for clinical trials. Their completion is critical for achieving the ultimate goal of curing patients with IPF.

Indexed as

nintedanibpirfenidonepulmonary fibrosistherapytreatment

Identifiers

PMID25767391
PMCPMC4354471
OpenAlexW1972319394

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.