Evidence map›Paper›PMID 39799434›Full record

ArticleClinical and translational medicine2025

CMPK2 promotes NLRP3 inflammasome activation via mtDNA-STING pathway in house dust mite-induced allergic rhinitis.

YaoMing Zheng, YaDong Xie, JiaYing Li, YuJie Cao, Min Li, Qing Cao, MiaoMiao Han, HongFei Lou, YiLai Shu, Hui Xiao and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
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  3. [cGAS-STING signaling pathway in Kawasaki disease: mechanistic insights and advances in clinical applications].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
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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.

YaoMing ZhengAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.ORCID 0000-0001-5267-3707
YaDong XieAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.
JiaYing LiAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.
YuJie CaoAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.
Min LiDepartment of Otolaryngology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Qing CaoAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.
MiaoMiao HanAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.
HongFei LouAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.
YiLai ShuEar Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.
Hui XiaoKey Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
HuaBin LiAllergy Center, Department of Otolaryngology, Affiliated Eye and ENT Hospital, Fudan University, Shanghai, China.

Funding

National Key R&D Program of China 2022YFC2504100National Natural Science Foundation of China 82101193National Natural Science Foundation of China 82271138
6 · The paper itself

Abstract

backgroundHouse dust mite (HDM) is the leading allergen for allergic rhinitis (AR). Although allergic sensitisation by inhaled allergens renders susceptible individuals prone to developing AR, the molecular mechanisms driving this process remain incompletely elucidated.

objectiveThis study aimed to elucidate the molecular mechanisms underlying HDM-induced AR.

methodsWe examined the expression of cytidine/uridine monophosphate kinase 2 (CMPK2), STING and the NLRP3 inflammasome in both AR patients and mice. Additionally, we investigated the role of CMPK2 and STING in the activation of the NLRP3 inflammasome in AR.

resultsThe expression of CMPK2, STING and the NLRP3 inflammasome was significantly increased in the nasal mucosa of AR patients compared to non-AR controls. A positive correlation was found between CMPK2 expression and the levels of STING, NLRP3, ASC, CASP1 and IL-1β. HDM treatment up-regulated the expression of CMPK2, and CMPK2 overexpression enhanced NLRP3 inflammasome activation in human nasal epithelial cells (HNEPCs). Additionally, mitochondrial reactive oxygen species (mtROS) production following HDM exposure contributed to mitochondrial dysfunction and the release of mitochondrial DNA (mtDNA), which activated the cyclic GMP-AMP synthase (cGAS)-STING pathway. Remarkably, depletion of mtDNA or inhibition of STING signalling reduced HDM-induced NLRP3 inflammasome activation in HNEPCs. In vivo, genetic knockout of CMPK2 or STING alleviated NLRP3 inflammasome activation and ameliorated clinical symptoms of AR in mice.

conclusionsOur results suggest that HDM promotes the activation of NLRP3 inflammasome through the up-regulation of CMPK2 and ensuing mtDNA-STING signalling pathway, hence revealing additional therapeutic target for AR. KEY POINTS: Cytidine/uridine monophosphate kinase 2 (CMPK2) expression is up-regulated in the nasal mucosa of patients and mice with allergic rhinitis (AR). CMPK2 caused NLRP3 inflammasome activation via mitochondrial DNA (mtDNA)-STING pathway. Blocking CMPK2 or STING signalling significantly reduced the activation of NLRP3 in house dust mite (HDM)-challenged mice and human nasal epithelial cells (HNEPCs).

Indexed as

DNA, MitochondrialInflammasomesMembrane ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinRhinitis, AllergicAdultAnimalsFemaleHumansMaleMicePyroglyphidaeSignal TransductionSTING ProteinDNA, MitochondrialInflammasomesMembrane ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanSTING1 protein, humanSting1 protein, mouseSTING Proteinallergic rhinitisCMPK2mitochondrial DNANLRP3 inflammasomeSTING

Identifiers

PMID39799434
PMCPMC11726638

What Socratic holds

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LicenceCC BY
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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.