Evidence map›Paper›PMID 29058630›Full record

ArticleBMC pulmonary medicine2017

Unsupervised gene expression analyses identify IPF-severity correlated signatures, associated genes and biomarkers.

Yunguan Wang, Jaswanth Yella, Jing Chen, Francis X McCormack, Satish K Madala, Anil G Jegga

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

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  10. Towards Treatable Traits for Pulmonary Fibrosis.Journal of personalized medicine · 2022
    Review
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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 2 institutions in 1 country.

Yunguan WangDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Jaswanth YellaDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Jing ChenDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Francis X McCormackDivision of Pulmonary, Critical Care and Sleep Medicine, University of Cincinnati, Cincinnati, OH, USA.
Satish K MadalaDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. satish.madala@cchmc.org.
Anil G JeggaDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. anil.jegga@cchmc.org.ORCID http://orcid.org/0000-0002-4881-7752
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

WT1 REGULATION OF PULMONARY FIBROSISR01HL134801 · NHLBI · UNIVERSITY OF CINCINNATI · PI MADALA, SATISH K · 2017 to 2025
$3.9M
Integrative analysis of multi-omics data to target fibroblast activation in IPFR21HL133539 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI JEGGA, ANIL, MADALA, SATISH K · 2016 to 2017
$248k
Discovery and characterization of candidate therapeutics for drug-induced pulmonary diseaseR21HL135368 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI JEGGA, ANIL · 2017 to 2018
$234k
NHLBI NIH HHS R01 HL134801NHLBI NIH HHS R21 HL133539NHLBI NIH HHS R21 HL135368
6 · The paper itself

Abstract

backgroundIdiopathic Pulmonary Fibrosis (IPF) is a fatal fibrotic lung disease occurring predominantly in middle-aged and older adults. The traditional diagnostic classification of IPF is based on clinical, radiological, and histopathological features. However, the considerable heterogeneity in IPF presentation suggests that differences in gene expression profiles can help to characterize and distinguish disease severity.

methodsWe used data-driven unsupervised clustering analysis, combined with a knowledge-based approach to identify and characterize IPF subgroups.

resultsUsing transcriptional profiles on lung tissue from 131 patients with IPF/UIP and 12 non-diseased controls, we identified six subgroups of IPF that generally correlated with the disease severity and lung function decline. Network-informed clustering identified the most severe subgroup of IPF that was enriched with genes regulating inflammatory processes, blood pressure and branching morphogenesis of the lung. The differentially expressed genes in six subgroups of IPF compared to healthy control include transcripts of extracellular matrix, epithelial-mesenchymal cell cross-talk, calcium ion homeostasis, and oxygen transport. Further, we compiled differentially expressed gene signatures to identify unique gene clusters that can segregate IPF from normal, and severe from mild IPF. Additional validations of these signatures were carried out in three independent cohorts of IPF/UIP. Finally, using knowledge-based approaches, we identified several novel candidate genes which may also serve as potential biomarkers of IPF.

conclusionsDiscovery of unique and redundant gene signatures for subgroups in IPF can be greatly facilitated through unsupervised clustering. Findings derived from such gene signatures may provide insights into pathogenesis of IPF and facilitate the development of clinically useful biomarkers.

Indexed as

TranscriptomeAgedBiomarkersCase-Control StudiesCluster AnalysisFemaleHumansIdiopathic Pulmonary FibrosisLogistic ModelsLungMaleMiddle AgedOligonucleotide Array Sequence AnalysisBiomarkersGene expression analysisGene signatureIdiopathic pulmonary fibrosisIpfIPF subtyping

Identifiers

PMID29058630
PMCPMC5649521
OpenAlexW2767051142

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.