Evidence map›Paper›PMID 25837031›Full record

ArticleThe European respiratory journal2015

The genetic basis of idiopathic pulmonary fibrosis.

Jonathan A Kropski, Timothy S Blackwell, James E Loyd

Open access · bronzeAbstract read
In one paragraph

Article in The European respiratory journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing 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

113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 193 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. Trial
  4. Article
  5. Article
  6. Altered cholesterol immunometabolism activates the macrophage NLRP3-inflammasome in lung fibrosis.American journal of respiratory cell and molecular biology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  13. Review
  14. Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Pulmonary fibrosis: from mechanisms to therapies.Journal of translational medicine · 2025
    Review

53 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jonathan A KropskiDivision of Allergy, Pulmonary and Critical Care Medicine, Dept of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA jon.kropski@vanderbilt.edu.
Timothy S BlackwellDivision of Allergy, Pulmonary and Critical Care Medicine, Dept of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA Dept of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA Dept of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA Department of Veterans Affairs Medical Center, Nashville, TN, USA.
James E LoydDivision of Allergy, Pulmonary and Critical Care Medicine, Dept of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
Vanderbilt University · US

Funding

Mechanisms of Familial Pulmonary FibrosisP01HL092870 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BLACKWELL, TIMOTHY S. · 2010 to 2020
$21.6M
Interdisciplinary Training Program in Lung ResearchT32HL094296 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ray Stokes Peebles · 2008 to 2026
$6.3M
Epithelial-Fibroblast Interactions in Lung FibrosisR01HL085317 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S. · 2007 to 2015
$3.5M
NHLBI NIH HHS HL085317NHLBI NIH HHS HL092870NHLBI NIH HHS HL94296NHLBI NIH HHS P01 HL092870NHLBI NIH HHS R01 HL085317NHLBI NIH HHS T32 HL094296
6 · The paper itself

Abstract

Throughout the past decade, there have been substantial advances in understanding the pathogenesis of idiopathic pulmonary fibrosis (IPF). Recently, several large genome-wide association and linkage studies have identified common genetic variants in more than a dozen loci that appear to contribute to IPF risk. In addition, family-based studies have led to the identification of rare genetic variants in genes related to surfactant function and telomere biology, and mechanistic studies suggest pathophysiological derangements associated with these rare genetic variants are also found in sporadic cases of IPF. Current evidence suggests that rather than existing as distinct syndromes, sporadic and familial cases of IPF (familial interstitial pneumonia) probably reflect a continuum of genetic risk. Rapidly evolving bioinformatic and molecular biology techniques, combined with next-generation sequencing technologies, hold great promise for developing a comprehensive, integrated approach to defining the fundamental molecular mechanisms that underlie IPF pathogenesis.

Indexed as

DNA HelicasesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansIdiopathic Pulmonary FibrosisIntracellular Signaling Peptides and ProteinsLung Diseases, InterstitialMucin-5BPulmonary Surfactant-Associated ProteinsTelomeraseDNA HelicasesIntracellular Signaling Peptides and ProteinsMUC5B protein, humanMucin-5BPulmonary Surfactant-Associated ProteinsRTEL1 protein, humanTelomeraseTERT protein, humanTOLLIP protein, human

Identifiers

PMID25837031
PMCPMC4849867
OpenAlexW2100190218

What OpenQuestion holds

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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.