Evidence map›Paper›PMID 41800242›Full record

ArticleInternational journal of biological sciences2026

Itaconate Modulates Neutrophil Homeostasis to Ameliorate Airway Inflammation in Diesel Exhaust Particles-exacerbated Asthma via Inhibiting NETs Formation.

Guiping Zhu, Ling Ye, Yansha Song, Yu Chen, Hui Cai, Zilinuer Abuduxukuer, Liping Zhu, Yingying Zeng, Wenjiao Zhu, Dan Ye and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 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

14 authors.

Guiping ZhuDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Ling YeDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yansha SongDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yu ChenDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Hui CaiDepartment of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Zilinuer AbuduxukuerDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Liping ZhuDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yingying ZengDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Wenjiao ZhuDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Dan YeMolecular and Cell Biology Lab, Institutes of Biomedical Sciences, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Yuanlin SongDepartment of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Pu WangMolecular and Cell Biology Lab, Institutes of Biomedical Sciences, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Meiling JinDepartment of Allergy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Jian WangDepartment of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Particulate matter exposure, especially diesel exhaust particles (DEP), can exacerbate neutrophilic airway inflammation which presents corticosteroid insensitivity, resulting in the loss of asthma control. The underlying biological mechanisms remain poorly understood, thereby impeding the development of innovative therapeutic strategies. Itaconate (ITA) is an anti-inflammatory metabolite that suppresses excessive immune activation in multiple pathological conditions. In this study, we identified that neutrophil acted as an essential regulator in DEP-induced corticosteroid-resistant asthma mouse models. Multi-omics and single-cell sequencing analysis found that aconitate decarboxylase 1 (ACOD1)/ITA was significantly elevated in neutrophils via the NF-κB signaling pathway in DEP-exacerbated asthma. Knockout of

Indexed as

AsthmaExtracellular TrapsInflammationNeutrophilsParticulate MatterSuccinatesVehicle EmissionsAnimalsCarboxy-LyasesHomeostasisHydro-LyasesMiceMice, Inbred C57BLMice, KnockoutAcod1 protein, mouseCarboxy-LyasesHydro-Lyasesitaconic acidParticulate MatterSuccinatesVehicle EmissionsCorticosteroid-resistant asthmaDiesel exhaust particlesItaconateNeutrophil extracellular trapsNeutrophils

Identifiers

PMID41800242
PMCPMC12965240

What OpenQuestion holds

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Registered trials

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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.