Evidence map›Paper›PMID 41158346›Full record

ArticleJournal of thoracic disease2025

Exploring diagnostic gene markers and immune infiltration in idiopathic pulmonary fibrosis.

Shuang Sun, Sibo Wang, Yuichi Sakairi, Giulia Maria Stella, Wei Zhao

Abstract read
In one paragraph

Article in Journal of thoracic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

5 authors.

Shuang Sun *The First Medical Center, Chinese PLA General Hospital, Beijing, China.
Sibo Wang *Chinese PLA Medical College, Beijing, China.ORCID https://orcid.org/0009-0007-5474-6675
Yuichi SakairiDepartment of General Thoracic Surgery, Chiba University Graduate School of Medicine, Chiba, Japan.
Giulia Maria StellaDepartment of Internal Medicine and Medical Therapeutics, University of Pavia Medical School, Pavia, Italy.
Wei ZhaoSenior Department of Respiratory and Critical Care Medicine, Chinese PLA General Hospital, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is one of the most severe pulmonary disorders, has poor outcomes, and is difficult to predict. This study sought to identify the critical genes involved in IPF progression, and to explore the relationship between these genes and immunogenic invasion. Methods: The GSE10667 dataset was downloaded from the Gene Expression Omnibus (GEO) database to identify differentially expressed genes (DEGs) between IPF patients and normal participants. IPF-related hub genes were screened using differential gene analysis and weighted gene co-expression network analysis (WGCNA). For evaluating the diagnostic efficacy of these hub genes, a nomogram was constructed, and receiver operating characteristic (ROC) analysis was performed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were conducted to explore the potential biological functions and pathways of the IPF-related hub genes. To reveal key protein-based genetic networks, protein-protein interaction (PPI) networks were constructed as follows: The key candidate genes associated with IPF, identified through WGCNA and differential gene analysis, were input into the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database, for PPI prediction and visualization. The PPI data derived from STRING were further processed and visualized using Cytoscape software. Additionally, the association between MMP2 and immune infiltration was analyzed. Finally, a Mendelian randomization (MR) analysis was performed using genome-wide association study (GWAS) data to establish the causal relationship between MMP2 and IPF. Results: In total, 486 DEGs in IPF were identified. A genetic co-expression network was established by the WGCNA to select the most relevant genes. The genes were mainly involved in processes such as the extracellular matrix (ECM), cellular aging, endoplasmic reticulum (ER) stress, and metalloproteinase (MT) activation signaling pathways. Crosslinks between the DEG-related modules and WGCNA modules were assessed to identify the key genes. A PPI network was then established that identified Conclusions:

Indexed as

Idiopathic pulmonary fibrosis (IPF)immune infiltrationMendelian randomization (MR)MMP2

Identifiers

PMID41158346
PMCPMC12557640

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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.