Evidence map›Paper›PMID 30660786›Full record

ReviewChest2019

Integrating Genomics Into Management of Fibrotic Interstitial Lung Disease.

Ayodeji Adegunsoye, Rekha Vij, Imre Noth

Open access · bronzeAbstract readReview
In one paragraph

Review in Chest, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
7.0field-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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. MitochondrialInternational journal of molecular sciences · 2025
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

3 authors at 2 institutions in 1 country.

Ayodeji AdegunsoyeSection of Pulmonary & Critical Care, Department of Medicine; The University of Chicago, Chicago, IL. Electronic address: deji@uchicago.edu.
Rekha VijSection of Pulmonary & Critical Care, Department of Medicine; The University of Chicago, Chicago, IL.
Imre NothDivision of Pulmonary & Critical Care & Sleep Medicine, Department of Medicine, University of Virginia, Charlottesville, VA.
University of Chicago · USUniversity of Virginia · US

Funding

Architectural structure and regulation of TOLLIP in IPFR01HL130796 · NHLBI · UNIVERSITY OF VIRGINIA · PI NOTH, IMRE · 2016 to 2019
$3.1M
NHLBI NIH HHS R01 HL130796
6 · The paper itself

Abstract

Fibrotic interstitial lung diseases (ILDs) have a high mortality rate with an unpredictable disease course and clinical features that frequently overlap. Recent data indicate important roles for genomics in the mechanisms underlying susceptibility and progression of pulmonary fibrosis. The impact of these genomic markers on pharmacotherapy and their contribution to outcomes is increasingly recognized. Interstitial lung abnormalities, frequently considered representative of early ILD, have been consistently associated with the MUC5B promoter polymorphism, a common gene variant. Other rare gene variant mutations, including TERT, TERC, SFTPC, and DKC1, may be present in patients with familial interstitial pneumonia and are frequently associated with a usual interstitial pneumonia pattern of fibrosis. The minor allele of the MUC5B rs35705950 genotype is prevalent in several sporadic forms of ILD, including idiopathic pulmonary fibrosis and chronic hypersensitivity pneumonitis. Gene mutations that characterize familial pulmonary fibrosis may be present in patients with connective tissue disease-related ILD, such as rheumatoid arthritis-ILD. Additionally, shorter telomere lengths and mutations in telomere biology-related genes have been demonstrated in both familial and sporadic ILD, with significant implications for disease progression, lung function, and survival. An improved understanding of the impact of genetic and genomic risk factors on disease progression would better guide personalized therapeutic choices in persons with fibrotic ILD.

Indexed as

Polymorphism, GeneticCause of DeathDisease ProgressionFemaleGenetic Predisposition to DiseaseGenotypeHumansImmunosuppressive AgentsLung Diseases, InterstitialMaleMolecular Targeted TherapyMucin-5BMutationPrognosisPromoter Regions, GeneticPulmonary FibrosisImmunosuppressive AgentsMucin-5Bgenegeneticsidiopathic interstitial pneumoniaidiopathic pulmonary fibrosisinterstitial lung disease

Identifiers

PMID30660786
PMCPMC6533453
OpenAlexW2910349372

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.