Evidence map›Paper›PMID 40950896›Full record

ArticleJournal of thoracic disease2025

Identification of the role of

Yilin Chen, Chengfei Xu, Dongchen Shi, Chengcheng Yang, Shulin Tong, Yi Qin, Wusheng Zhang, Xiang Li, Sen Tian, Yuchao Dong and 2 more

Abstract read
PubMed Full text at PMC Publisher
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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

12 authors.

Yilin Chen *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Chengfei Xu *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Dongchen Shi *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Chengcheng YangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Shulin TongDepartment of Respiratory and Critical Care Medicine, No. 990 Hospital of the Chinese People's Liberation Army Joint Logistic Support Force, Zhumadian, China.
Yi QinDepartment of Respiratory and Critical Care Medicine, No. 990 Hospital of the Chinese People's Liberation Army Joint Logistic Support Force, Zhumadian, China.
Wusheng ZhangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Xiang LiDepartment of Respiratory and Critical Care Medicine, General Hospital of Central Theater Command of Chinese People's Liberation Army, Wuhan, China.
Sen TianDepartment of Respiratory and Critical Care Medicine, No. 906 Hospital of the Chinese People's Liberation Army Joint Logistic Support Force, Ningbo, China.
Yuchao DongDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Hui ShiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Chong BaiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Benign airway stenosis (BAS) is a disease characterized by the formation of fibrotic tissue leading to airway stenosis with unclear underlying molecular mechanisms. This study aimed to identify the key genes regulating fibrosis in BAS. Methods: In this study, the fibrotic mechanism of BAS was explored through combined transcriptomic and proteomic analysis. We collected tracheal samples from day 7 of a mouse model of BAS, as well as from normal control mice. These samples underwent transcriptomic and proteomic sequencing, followed by integrative analysis to identify key genes associated with the condition. Subsequently, we assessed airway fibrosis in the BAS model mice after treatment with an inhibitor targeting the identified gene. Results: The analysis revealed 4,336 significantly differentially expressed genes (DEGs) at the transcriptomic level and 1,634 differentially expressed proteins (DEPs) at the proteomic level. Through cross-omics integrative analysis, 195 upregulated genes [designated as correlated DEGs and DEPs (cor-DEGs-DEPs)] exhibited significant concordance in expression patterns at both messenger RNA (mRNA) and protein levels, forming differentially co-expressed gene-protein pairs. Utilizing a combined analysis of transcriptomics and proteomics, we identified the Conclusions:

Indexed as

ARG1Benign airway stenosis (BAS)fibrosisproteome sequencingtranscriptome sequencing

Identifiers

PMID40950896
PMCPMC12433044

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.