Evidence map›Paper›PMID 27303645›Full record

ReviewF1000Research2016

Recent advances in understanding idiopathic pulmonary fibrosis.

Cécile Daccord, Toby M Maher

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in F1000Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
11.5field-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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Systematic review of drug effects in humans and models with surfactant-processing disease.European respiratory review : an official journal of the European Respiratory Society · 2018
    Pooled it
  3. Review
  4. The intersection of liver cirrhosis and pulmonary fibrosis.Journal of translational medicine · 2025
    Review
  5. Review
  6. Air pollution and alveolar health.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  7. CD45+/ Col I+ Fibrocytes: Major source of collagen in the fibrotic lung, but not in passaged fibroblast cultures.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Article
  8. Review
  9. Prognostic value of [Scientific reports · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Small Airways in Idiopathic Pulmonary Fibrosis: Quiet but Not Forgotten.American journal of respiratory and critical care medicine · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. 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

2 authors at 1 institution in 2 countries.

Cécile DaccordInterstitial Lung Disease Unit, Royal Brompton and Harefield NHS Foundation Trust, London, UK; Respiratory Medicine Department, Lausanne University Hospital, Lausanne, Switzerland.
Toby M MaherInterstitial Lung Disease Unit, Royal Brompton and Harefield NHS Foundation Trust, London, UK; NIHR Respiratory Biomedical Research Unit, Royal Brompton Hospital, London, UK; Fibrosis Research Group, Imperial College, London, UK.
Royal Brompton & Harefield NHS Foundation Trust · GB

Funding

Department of Health CS-2013-13-017HSRD VA CDA 13-017
6 · The paper itself

Abstract

Despite major research efforts leading to the recent approval of pirfenidone and nintedanib, the dismal prognosis of idiopathic pulmonary fibrosis (IPF) remains unchanged. The elaboration of international diagnostic criteria and disease stratification models based on clinical, physiological, radiological, and histopathological features has improved the accuracy of IPF diagnosis and prediction of mortality risk. Nevertheless, given the marked heterogeneity in clinical phenotype and the considerable overlap of IPF with other fibrotic interstitial lung diseases (ILDs), about 10% of cases of pulmonary fibrosis remain unclassifiable. Moreover, currently available tools fail to detect early IPF, predict the highly variable course of the disease, and assess response to antifibrotic drugs. Recent advances in understanding the multiple interrelated pathogenic pathways underlying IPF have identified various molecular phenotypes resulting from complex interactions among genetic, epigenetic, transcriptional, post-transcriptional, metabolic, and environmental factors. These different disease endotypes appear to confer variable susceptibility to the condition, differing risks of rapid progression, and, possibly, altered responses to therapy. The development and validation of diagnostic and prognostic biomarkers are necessary to enable a more precise and earlier diagnosis of IPF and to improve prediction of future disease behaviour. The availability of approved antifibrotic therapies together with potential new drugs currently under evaluation also highlights the need for biomarkers able to predict and assess treatment responsiveness, thereby allowing individualised treatment based on risk of progression and drug response. This approach of disease stratification and personalised medicine is already used in the routine management of many cancers and provides a potential road map for guiding clinical care in IPF.

Indexed as

idiopathic pulmonary fibrosisinterstitial lung diseases

Identifiers

PMID27303645
PMCPMC4890320
OpenAlexW2413462878

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.