Evidence map›Paper›PMID 26595739›Full record

ArticleAnnals of the American Thoracic Society2015

MUC5B and Idiopathic Pulmonary Fibrosis.

Ivana V Yang, Tasha E Fingerlin, Christopher M Evans, Marvin I Schwarz, David A Schwartz

Open access · greenAbstract read
In one paragraph

Article in Annals of the American Thoracic Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 6% 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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

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  18. Microscopic Small Airway Abnormalities Identified in Early Idiopathic Pulmonary FibrosisAmerican journal of respiratory and critical care medicine · 2024
    Article
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  20. Article

4 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

5 authors at 2 institutions in 1 country.

Ivana V Yang1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
Tasha E Fingerlin3 Center for Genes, Environment, and Health, National Jewish Health, Denver, Colorado.
Christopher M Evans1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
Marvin I Schwarz1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
David A Schwartz1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
University of Colorado Denver · USColorado School of Public Health · 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
Role of Mucin in Lung Homeostasis and PathophysiologyR01HL080396 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Christopher M Evans · 2009 to 2026
$8.6M
Functional Genetics in Idiopathic Pulmonary FibrosisR33HL120770 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SCHWARTZ, DAVID ALBERT · 2016 to 2018
$1.6M
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 HL080396NHLBI NIH HHS R01 HL097163NHLBI NIH HHS R21 HL121572NHLBI NIH HHS R33 HL120770
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF), a fatal disease that is a result of complex interactions between genetics and the environment, has limited treatment options. We have identified the MUC5B promoter polymorphism and other common genetic variants that in aggregate explain roughly one-third of disease risk. The MUC5B promoter polymorphism is the strongest and the most replicated genetic risk factor for IPF, appears to be protective and predictive in this disease, and is likely involved in disease pathogenesis through an increase in MUC5B expression in terminal bronchi and honeycombed cysts. Expression of MUC5B is also highly correlated with expression of cilium genes in IPF lung. Our work suggests that mucociliary dysfunction in the distal airway may play a role in the development of progressive fibroproliferative lung disease. In addition, our work has important implications for secondary prevention, early detection, and future early and personalized treatment based on genetic profiles.

Indexed as

Promoter Regions, GeneticGenetic Predisposition to DiseaseGenetic VariationHumansIdiopathic Pulmonary FibrosisLungMucin-5BMUC5B protein, humanMucin-5Bgene expression profileMUC5Bmucociliary dysfunctionpulmonary fibrosis; genetic variant

Identifiers

PMID26595739
PMCPMC4722833
OpenAlexW2178655245

What OpenQuestion holds

Textmetadata
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.