Evidence map›Paper›PMID 37181377›Full record

ReviewFrontiers in medicine2023

Idiopathic pulmonary fibrosis and the role of genetics in the era of precision medicine.

Aitana Alonso-Gonzalez, Eva Tosco-Herrera, Maria Molina-Molina, Carlos Flores

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
6.7field-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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Multi-omics insights into the mechanisms and prognosis of IPF.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
    Review
  5. Review
  6. Post-lung transplant surveillance in 2026: current practice, variability, and the need for standardization.Transplant international : official journal of the European Society for Organ Transplantation · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Highlights on Future Treatments of IPF: Clues and Pitfalls.International journal of molecular sciences · 2024
    Review
  17. Genetics of chronic respiratory disease.Nature reviews. Genetics · 2024
    Review
  18. A Test to Comprehensively Capture the Known Genetic Component of Familial Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2024
    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

4 authors at 3 institutions in 1 country.

Aitana Alonso-GonzalezUnidad de Investigación, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Eva Tosco-HerreraUnidad de Investigación, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Maria Molina-MolinaServei de Pneumologia, Laboratori de Pneumologia Experimental, IDIBELL, Barcelona, Spain.
Carlos FloresUnidad de Investigación, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Hospital Universitario Nuestra Señora de Candelaria · ESInstitut d'Investigació Biomédica de Bellvitge · ESUniversidade de Santiago de Compostela · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, rare progressive lung disease, characterized by lung scarring and the irreversible loss of lung function. Two anti-fibrotic drugs, nintedanib and pirfenidone, have been demonstrated to slow down disease progression, although IPF mortality remains a challenge and the patients die after a few years from diagnosis. Rare pathogenic variants in genes that are involved in the surfactant metabolism and telomere maintenance, among others, have a high penetrance and tend to co-segregate with the disease in families. Common recurrent variants in the population with modest effect sizes have been also associated with the disease risk and progression. Genome-wide association studies (GWAS) support at least 23 genetic risk loci, linking the disease pathogenesis with unexpected molecular pathways including cellular adhesion and signaling, wound healing, barrier function, airway clearance, and innate immunity and host defense, besides the surfactant metabolism and telomere biology. As the cost of high-throughput genomic technologies continuously decreases and new technologies and approaches arise, their widespread use by clinicians and researchers is efficiently contributing to a better understanding of the pathogenesis of progressive pulmonary fibrosis. Here we provide an overview of the genetic factors known to be involved in IPF pathogenesis and discuss how they will continue to further advance in this field. We also discuss how genomic technologies could help to further improve IPF diagnosis and prognosis as well as for assessing genetic risk in unaffected relatives. The development and validation of evidence-based guidelines for genetic-based screening of IPF will allow redefining and classifying this disease relying on molecular characteristics and contribute to the implementation of precision medicine approaches.

Indexed as

exome sequencinggenetic testingIdiopathic pulmonary fibrosisprecision medicinetelomere length

Identifiers

PMID37181377
PMCPMC10172674
OpenAlexW4367294662

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.