Evidence map›Paper›PMID 41952982›Full record

ArticleiScience2026

KAT8 drives M2 macrophage polarization to exacerbate allergic airway inflammation.

Xianwen Lai, Han Li, Zhao Zhao, Yu Zhong, Guomei Su, Jiewen Huang, Yuanyuan Xiang, Ruina Huang, Jingyun Quan, Zhihang Feng and 9 more

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PubMed Full text at PMC Publisher
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Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

19 authors.

Xianwen LaiDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Han LiDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Zhao ZhaoDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Yu ZhongSchool of Ocean and Tropical Medicine. Guangdong Medical University, Zhanjiang, Guangdong 524023, China.
Guomei SuDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Jiewen HuangDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Yuanyuan XiangDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Ruina HuangDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Jingyun QuanDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Zhihang FengDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Zhenfu FangDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Shihai LiClinical Research Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Tong HuangSchool of Basic Medicine, Guangdong Medical University, Dongguan 523808, China.
Zhiling XiongDepartment of Geriatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Yuting LeiDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Wenchao ZhangDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Jielin DuanDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.
Xiao GaoInstitute of Respiratory Diseases, The Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Tianwen LaiDongguan Key Laboratory of Immune Inflammation and Metabolism, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan 523121, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated macrophage polarization is a pivotal driver of airway inflammation in asthma, yet the underlying molecular mechanisms remain incompletely understood. Here, we demonstrate that histone acetyltransferase KAT8 exacerbates allergic airway inflammation by promoting M2 macrophage polarization in asthma. KAT8 expression was significantly upregulated in lung macrophages of asthmatic mice and in bone marrow-derived macrophages (BMDMs) stimulated with house dust mite (HDM). Macrophage-specific KAT8 deficiency attenuated allergic airway inflammation and inhibited M2 macrophage polarization by suppressing signal transducer and activator of transcription 3 (STAT3) signaling. Mechanistically, KAT8 directly interacted with STAT3 and targeted it for acetylation, thereby driving M2 macrophage polarization. Importantly, pharmacological inhibition of KAT8 reduced M2 macrophage polarization and attenuated allergic airway inflammation. These findings establish KAT8 as a critical regulator of macrophage-driven allergic inflammation via STAT3 acetylation, highlighting its potential as a therapeutic target for asthma.

Indexed as

biological sciencesimmunologyrespiratory medicine

Identifiers

PMID41952982
PMCPMC13053759

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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.