Evidence map›Paper›PMID 24746870›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2015

Epigenetics of idiopathic pulmonary fibrosis.

Ivana V Yang, David A Schwartz

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
8.5field-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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Multi-omics insights into the mechanisms and prognosis of IPF.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
    Review
  3. Review
  4. Article
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  6. Article
  7. Review
  8. Air pollution and alveolar health.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Discovery of Pyrrolo[2,3-ACS medicinal chemistry letters · 2023
    Article
  14. Review
  15. Article
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  20. Article

12 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

2 authors at 2 institutions in 1 country.

Ivana V YangDepartment of Medicine, University of Colorado School of Medicine, Aurora, Colo; Department of Epidemiology, Colorado School of Public Health, Aurora, Colo. Electronic address: ivana.yang@yahoo.com.
David A SchwartzDepartment of Medicine, University of Colorado School of Medicine, Aurora, Colo; Department of Immunology, University of Colorado School of Medicine, Aurora, Colo.
Colorado School of Public Health · USUniversity of Colorado Denver · US

Funding

Role of Genetics in Idiopathic Pulmonary Fibrosis (IPF)R01HL097163 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI FINGERLIN, TASHA E., SCHWARTZ, DAVID ALBERT · 2009 to 2018
$16.4M
Lung Genomics Research ConsortiumRC2HL101715 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI GERACI, MARK W, KAMINSKI, NAFTALI · 2009 to 2010
$11.4M
Genomic Signatures for Idiopathic Interstitial PneumoniaR01HL095393 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SCHWARTZ, DAVID ALBERT · 2008 to 2011
$3.3M
Regulation of mRNA and miRNA Expression in Pulmonary Fibrosis by DNA MethylationR21HL121572 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI YANG, IVANA V · 2014 to 2015
$231k
NHLBI NIH HHS R01 HL095393NHLBI NIH HHS R01 HL097163NHLBI NIH HHS R21 HL121572
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a complex lung disease of unknown etiology. Development of IPF is influenced by both genetic and environmental factors. Recent work by our and other groups has identified strong genetic predisposition factors for the development of pulmonary fibrosis, and cigarette smoke remains the most strongly associated environmental exposure risk factor. Gene expression profiling studies of IPF lung have taught us quite a bit about the biology of this fatal disease, and those of peripheral blood have provided important biomarkers. However, epigenetic marks may be the missing link that connects the environmental exposure in genetically predisposed individuals to transcriptional changes associated with disease development. Moreover, epigenetic marks represent a promising therapeutic target for IPF. In this review, the disease is introduced, genetic and gene expression studies in IPF are summarized, exposures relevant to IPF and known epigenetic changes associated with cigarette smoke exposure are discussed, and epigenetic studies conducted so far in IPF are summarized. Limitations, challenges, and future opportunities in this field are also discussed.

Indexed as

Epigenesis, GeneticAnimalsEnvironmental ExposureGenetic Predisposition to DiseaseHumansIdiopathic Pulmonary FibrosisMicroRNAsRisk FactorsSmokingTranslational Research, BiomedicalMicroRNAs

Identifiers

PMID24746870
PMCPMC4182166
OpenAlexW2053648326

What OpenQuestion holds

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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.