Evidence map›Paper›PMID 39668431›Full record

ArticleAnimal models and experimental medicine2025

Deficiency of DEK proto-oncogene alleviates allergic rhinitis by inhibiting RhoA/Ezrin-mediated mitochondrial fission.

Longzhu Dai, Yongde Jin, Jingmei Chai, Jianing Yang, Jiangang Wang, Mu Chen, Liangchang Li, Chongyang Wang, Guanghai Yan

Abstract read
In one paragraph

Article in Animal models and experimental medicine, 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

9 authors.

Longzhu DaiJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Yongde JinJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Jingmei ChaiJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Jianing YangJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Jiangang WangJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Mu ChenJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Liangchang LiJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Chongyang WangJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.
Guanghai YanJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, P. R. China.ORCID 0000-0001-8058-7822

Funding

National Natural Science Foundation of China 82260007National Natural Science Foundation of China 82260218Natural Science Research Foundation of Jilin Province for Sciences and Technology 20210101215JCNatural Science Research Foundation of Jilin Province for Sciences and Technology 20240404025ZPNatural Science Research Foundation of Jilin Province for Sciences and Technology 20240602100RCThe Department of Education of Jilin Province (JJKH20240698KJ);
6 · The paper itself

Abstract

backgroundAllergic rhinitis (AR) is a kind of immune disease mediated by IgE. We are intrigued by the potential role of DEK proto-oncogene (DEK) in inflammation-related diseases. We investigated the effects and mechanisms of DEK in treating AR, aiming to identify potential new treatment targets for AR.

methodsThe AR mouse model was induced by house dust mite (HDM) (1 mg/mL). HNEpCs stimulated by HDM (1 mg/mL) were pretreated for 24 h with or without DEK lentivirus. The effect of DEK knockout or knockdown on AR was evaluated in vitro and in vivo using western blotting, ELISA, flow cytometry, real-time quantitative PCR, immunohistochemistry, HE staining, PAS staining, Diff staining, and immunofluorescence.

resultsAfter DEK knockdown, the inflammatory response of AR mice was reduced. In addition, DEK deletion mitigated nasal tissue damage and mitochondrial division. Our further studies showed that DEK deletion or inhibition led to the down-regulation of RhoA activity and decreased phosphorylation of Ezrin and Drp1 proteins, and inhibited mitochondrial division. Overall, DEK deficiency mitigated AR by down-regulating RhoA/Ezrin/Drp1 pathway activity.

conclusionDEK alleviates AR through RhoA/Ezrin/Drp1 signaling pathway, which provides a new perspective for developing improved therapies and understanding the pathogenesis of AR.

Indexed as

Chromosomal Proteins, Non-HistoneCytoskeletal ProteinsMitochondrial DynamicsOncogene ProteinsPoly-ADP-Ribose Binding ProteinsRhinitis, AllergicrhoA GTP-Binding ProteinAnimalsDisease Models, AnimalDNA-Binding ProteinsEzrinMaleMiceMice, KnockoutProto-Oncogene MasPyroglyphidaeChromosomal Proteins, Non-HistoneCytoskeletal ProteinsDEK protein, mouseDNA-Binding ProteinsEzrinMAS1 protein, humanOncogene ProteinsPoly-ADP-Ribose Binding ProteinsProto-Oncogene MasrhoA GTP-Binding ProteinRhoA protein, mouseallergic rhinitisDEKEzrinhouse dust mitemitochondria

Identifiers

PMID39668431
PMCPMC12746191

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.