Evidence map›Paper›PMID 42381528›Full record

ArticleJournal of Korean medical science2026

EGFR and Its Ligands in Idiopathic Pulmonary Fibrosis: Predicting Clinical Outcomes and Molecular Endotyping Through In-Depth Analysis.

Jong-Uk Lee, Seung-Lee Park, Min Kyung Kim, Eun-Jeong Seo, Hun-Gyu Hwang, Beomseok Son, Tae Rim Kim, Han-Oh Park, June Young Park, Hun Soo Chang and 1 more

Abstract read
In one paragraph

Article in Journal of Korean medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Jong-Uk Lee *Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang University, Asan, Korea.ORCID https://orcid.org/0000-0002-0232-5381
Seung-Lee Park *Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang University, Asan, Korea.ORCID https://orcid.org/0000-0002-1562-732X
Min Kyung KimDepartment of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang University, Asan, Korea.ORCID https://orcid.org/0000-0003-2996-0198
Eun-Jeong SeoDepartment of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang University, Asan, Korea.ORCID https://orcid.org/0009-0000-9347-0244
Hun-Gyu HwangDivision of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea.ORCID https://orcid.org/0000-0001-9304-7219
Beomseok SonsiRNAgen Therapeutics, Cambridge, MA, USA.ORCID https://orcid.org/0000-0003-3977-425X
Tae Rim KimsiRNAgen Therapeutics, Cambridge, MA, USA.ORCID https://orcid.org/0000-0002-2682-8813
Han-Oh ParksiRNAgen Therapeutics, Cambridge, MA, USA.ORCID https://orcid.org/0000-0002-5053-9018
June Young ParkCenos Therapeutics, San Carlos, CA, USA.ORCID https://orcid.org/0000-0001-8688-0907
Hun Soo ChangDepartment of Microbiology, College of Medicine, Soonchunhyang University, Cheonan, Korea. hschang@sch.ac.kr.ORCID https://orcid.org/0000-0002-4025-4182
Choon-Sik ParkDivision of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea. mdcspark@daum.net.ORCID https://orcid.org/0000-0003-2977-0255

Funding

National Research Foundation of Korea RS-2023-00240858
6 · The paper itself

Abstract

backgroundThe dysregulation of alveolar epithelial cells has been proposed as the cause of idiopathic pulmonary fibrosis (IPF) due to abnormal activation of epidermal growth factor receptor (EGFR). However, the ways of interaction with EGFR ligands including amphiregulin (AREG), epidermal growth factor (EGF), transforming growth factor (TGF)-α and heparin-binding EGF have not been revealed. The aim of the present study was to investigate the diagnostic and prognostic significance of EGFR and its ligands in IPF.

methodsEGFR and its ligands were quantified by enzyme-linked immunosorbent assay in bronchoalveolar lavage (BAL) fluids and serum from 131 patients with IPF and 52 normal controls (NCs). Mortality risk was evaluated using Cox proportional hazards models. Cluster analysis based on EGFR and its ligands was conducted using both hierarchical and K-means clustering methods.

resultsThe patients exhibited significantly higher levels of EGFR, AREG, EGF, and TGF-α compared to NCs. The threshold values for AREG, EGF and TGF-α were determined to be 12.2 pg/mL, 6.3 pg/mL and 5.2 pg/mL, respectively, for the two groups. The sensitivities were 79.83%, 88.24%, and 56.30%, and the specificities were 81.82%, 31.82%, and 63.64% to diagnose IPF, respectively. The mortality rate was significantly higher in IPF patients with low levels compared to those with high levels of EGFR and EGF on Cox analysis. Four distinct clusters were identified based on the levels of EGFR and its ligands in BAL fluids. C3 group (n = 7), which exhibited the highest levels of TGF-α, AREG and EGFR, showed the highest risk of mortality, whereas the C2 group (n = 40), with the highest level of EGF and the intermediate levels of AREG, EGFR, and TGF-α, had the lowest risk.

conclusionThe diverse effects of EGFR on mortality may depend on balance of TGF-α and EGF. Therefore, a comprehensive analysis of EGFR and its ligands could help predict molecular endotypes and clinical outcomes for IPF patients.

Indexed as

ErbB ReceptorsIdiopathic Pulmonary FibrosisAgedAmphiregulinBronchoalveolar Lavage FluidCase-Control StudiesCluster AnalysisEnzyme-Linked Immunosorbent AssayEpidermal Growth FactorFemaleHeparin-binding EGF-like Growth FactorHumansKaplan-Meier EstimateLigandsMaleMiddle AgedAmphiregulinAREG protein, humanEGFR protein, humanEpidermal Growth FactorErbB ReceptorsHeparin-binding EGF-like Growth FactorLigandsTransforming Growth Factor alphaClusteringEGF ReceptorEGF Receptor LigandsIdiopathic Pulmonary Fibrosis

Identifiers

PMID42381528
PMCPMC13320476

What OpenQuestion holds

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LicenceCC BY-NC
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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.