Evidence map›Paper›PMID 41732344›Full record

ArticleThe World Allergy Organization journal2026

IFITM1 is required for epithelial mesenchymal transition in airway remodeling of allergic asthma.

Manni Zhu, Xiaoqin Weng, Chuanli Zhang, Xiaofei Song, Shan Liu, Tingting Xu, Zhengxia Wang, Zhongqi Chen, Mingshun Zhang, Mao Huang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The World Allergy Organization journal, 2026. 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

11 authors.

Manni ZhuDepartment of Respiratory and Critical Care Medicine, Nantong First People's Hospital, Nantong, China.
Xiaoqin WengDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Chuanli ZhangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xiaofei SongDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Shan LiuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Tingting XuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhengxia WangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhongqi ChenDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mingshun ZhangJiangsu Province Engineering Research Center of Antibody Drug, NHC Key Laboratory of Antibody Technique, Department of Immunology, Nanjing Medical University, Nanjing, China.
Mao HuangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ningfei JiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Interferon-induced transmembrane protein 1 (IFITM1) restricts virus infection. IFITM proteins are involved in Th2 cell differentiation in allergic asthma. The epithelial‒mesenchymal transition (EMT) regulates allergic airway remodeling. We sought to explore the functional contributions and underlying mechanisms of IFITM1 in the EMT associated with allergic asthma. Methods: The expression of IFITM1 was measured in pulmonary tissues from asthma patients and in a house dust mite (HDM)-induced murine asthma model. The mechanisms by which IFITM1 affects the EMT of airway remodeling were investigated Results: We demonstrated that airway IFITM1 was increased in patients with asthma. As expected, HDM exposure increased airway IFITM1 in an asthmatic murine model. The increase in IFITM1 was mediated through IFN-β stimulation and subsequent STAT1 signaling activation. Blocking IFNAR or knocking down Conclusion: IFIMT1, which is upregulated in airway epithelial cells via the IFN-β and STAT1 signaling pathways, contributes to EMT during allergic airway remodeling and may serve as a potential treatment target for allergic asthma.

Indexed as

Airway remodelingAsthmaEpithelial-mesenchymal transitionInterferon induced transmembrane protein 1Interleukin-17Tnc protein

Identifiers

PMID41732344
PMCPMC12925070

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.