Evidence map›Paper›PMID 31423451›Full record

ArticleERJ open research2019

RNA sequencing of transplant-stage idiopathic pulmonary fibrosis lung reveals unique pathway regulation.

Pitchumani Sivakumar, John Ryan Thompson, Ron Ammar, Mary Porteous, Carly McCoubrey, Edward Cantu, Kandasamy Ravi, Yan Zhang, Yi Luo, Denis Streltsov and 3 more

Open access · goldAbstract read
In one paragraph

Article in ERJ open research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  13. Adiponectin suppresses stiffness-dependent, profibrotic activation of lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2024
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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

13 authors at 4 institutions in 1 country.

Pitchumani SivakumarFibrosis Translational Research and Development, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
John Ryan ThompsonTranslational Bioinformatics, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
Ron AmmarTranslational Bioinformatics, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
Mary PorteousPulmonary and Critical Care Medicine, University of Pennsylvania, Philadelphia PA, USA.
Carly McCoubreyPulmonary and Critical Care Medicine, University of Pennsylvania, Philadelphia PA, USA.
Edward CantuSurgery Dept, University of Pennsylvania, Philadelphia PA, USA.
Kandasamy RaviIntegrated Genomics, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
Yan ZhangIntegrated Genomics, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
Yi LuoClinical Biomarkers, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
Denis StreltsovFibrosis Translational Research and Development, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
Michael F BeersPulmonary and Critical Care Medicine, University of Pennsylvania, Philadelphia PA, USA.
Gabor JaraiFibrosis Translational Research and Development, Bristol-Myers Squibb Research and Development, Princeton NJ, USA.
Jason D ChristiePulmonary and Critical Care Medicine, University of Pennsylvania, Philadelphia PA, USA.
Bristol-Myers Squibb (United States) · USUniversity of Pennsylvania · USIgenbio (United States) · USPenn Center for AIDS Research · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Trevor M Penning · 2006 to 2026
$35.3M
Surfactant Protein C Mutations:Interstitial Lung DiseaseR01HL074064 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BEERS, MICHAEL FRANCIS · 2003 to 2006
$1.8M
NHLBI NIH HHS R01 HL074064NIEHS NIH HHS P30 ES013508
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF), the scarring of lung parenchyma resulting in the loss of lung function, remains a fatal disease with a significant unmet medical need. Patients with severe IPF often develop acute exacerbations resulting in the rapid deterioration of lung function, requiring transplantation. Understanding the pathophysiological mechanisms contributing to IPF is key to develop novel therapeutic approaches for end-stage disease. We report here RNA-sequencing analyses of lung tissues from a cohort of patients with transplant-stage IPF (n=36), compared with acute lung injury (ALI) (n=11) and nondisease controls (n=19), that reveal a robust gene expression signature unique to end-stage IPF. In addition to extracellular matrix remodelling pathways, we identified pathways associated with T-cell infiltration/activation, tumour development, and cholesterol homeostasis, as well as novel alternatively spliced transcripts that are differentially regulated in the advanced IPF lung

Identifiers

PMID31423451
PMCPMC6689672
OpenAlexW2968769612

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.