Evidence map›Paper›PMID 41437357›Full record

ArticleRespiratory research2025

CPA3 drives the development of asthma by promoting the activation of the JAK/STAT6 pathway.

Ke Wang, Ruhao Wu, Mingwei Fan, Ruohan Jia, Yize Liu, Yue Li, Pengfei Li, Yu Wang, Tianci Jiang, Zhe Cheng

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In one paragraph

Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
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

10 authors.

Ke Wang *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Ruhao Wu *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Mingwei Fan *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Ruohan JiaDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Yize LiuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Yue LiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Pengfei LiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Yu WangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Tianci JiangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Zhe ChengDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China. fccchengzhe@zzu.edu.cn.

Funding

National Natural Science Foundation of China 82170037
6 · The paper itself

Abstract

backgroundAsthma is a prevalent chronic respiratory disease that affects lots of people all over the world. Characterized by multiple complex mechanisms, asthma poses substantial challenges for both patients and healthcare providers in clinical management. Comprehending the underlying mechanisms that drive the onset and progression of asthma is crucial for developing effective therapies.

methodsThe expression of CPA3 was analyzed via bioinformatics, and bulk RNA-seq datasets were utilized for this purpose. The findings were validated using quantitative real-time PCR and western blotting. A house dust mite–induced asthma mouse model was established to evaluate CPA3 expression in airway epithelial cells. Furthermore, the BEAS-2B cell line was used to investigate the potential mechanisms by which CPA3 contributes to the pathogenesis and progression of asthma.

resultsWe identified four key genes from DEGs and module genes from WGCNA based on RNA-seq data of asthma. Applying random forest algorithm, we focus on CPA3 as the most significant gene in asthma diagnosis. Afterwards, we detected higher level of CPA3 in BEAS-2B asthma model and asthma mice model. Besides, we proved CPA3 might activate STAT6 phosphorylation through JAK/STAT6 pathway.

conclusionThis study has provided comprehensive insights into the molecular mechanisms underlying asthma and has identified CPA3 as a potential biomarker for the condition. In BEAS-2B cells, CPA3 has been shown to drive asthma progression by activating the JAK/STAT6 pathway, a process that can be inhibited using leflunomide.

Indexed as

AsthmaJanus KinasesSTAT6 Transcription FactorAnimalsCell LineDisease Models, AnimalFemaleHumansMiceMice, Inbred BALB CSignal TransductionJanus KinasesSTAT6 Transcription FactorAirway epithelial cellsAsthmaBulk RNA sequencingCPA3Differentially expressed genes

Identifiers

PMID41437357
PMCPMC12836841

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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.