Evidence map›Paper›PMID 42337539›Full record

ArticleRespiratory research2026

H3K18 lactylation promotes allergic airway inflammation in asthma via a CSF1/CSF1R/MAPK autocrine axis.

Minxuan Hu, Yixin Chen, Haohua Huang, Jinzhong Zhuo, Haishan Zhong, Dongyu Liu, Qi Yu, Yuhan Du, Jinming Zhang, Shaoxi Cai and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 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

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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. Review
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.

Minxuan Hu *Chronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yixin Chen *Chronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Haohua HuangChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jinzhong ZhuoChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Haishan ZhongChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Dongyu LiuChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Qi YuChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuhan DuChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jinming ZhangChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Shaoxi CaiChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China. hxkc@smu.edu.cn.
Hangming DongChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China. dhm@smu.edu.cn.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2024B1515120044National Natural Science Foundation of China 82170032
6 · The paper itself

Abstract

backgroundMetabolic reprogramming of airway epithelial cells is a hallmark of asthma, yet the mechanisms by which altered metabolism drives inflammation remain largely unknown. Histone lactylation, a recently identified metabolism-derived epigenetic modification, may provide a mechanistic link.

methodsClinical specimens and single-cell RNA sequencing (scRNA-seq) were analyzed to map the metabolic landscape of asthma. Histone lactylation in airway epithelial cells was assessed by western blotting and immunofluorescence. Functional roles of histone lactylation were evaluated via modulation of glycolysis, lactate availability, or P300 expression. Chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq) were performed to identify transcriptional targets of H3K18 lactylation (H3K18la).

resultsGlycolysis and histone lactylation, particularly H3K18la, were significantly elevated in the airway epithelial cells of asthma. Inhibition of glycolysis or P300 knockdown attenuated the inflammatory response by suppressing histone lactylation; whereas lactate supplementation exacerbated inflammation by promoting histone lactylation. H3K18la accumulated at the CSF1R promoter, directly enhancing its transcription and establishing a CSF1/CSF1R/MAPK autocrine positive feedback axis that positions airway epithelial cells as an upstream driver and inflammatory amplifier in allergic airway inflammation.

conclusionThis study defines a glycolysis-histone lactylation-CSF1R signaling axis that links epithelial metabolic reprogramming to sustained inflammatory gene activation in asthma, highlighting histone lactylation as a potential therapeutic target for allergic airway inflammation.

Indexed as

AsthmaAutocrine CommunicationHistonesMacrophage Colony-Stimulating FactorMAP Kinase Signaling SystemReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAnimalsEpithelial CellsFemaleHumansMiceReceptor, Macrophage Colony-Stimulating FactorCSF1R protein, humanHistonesMacrophage Colony-Stimulating FactorReceptor, Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAllergic airway inflammationAsthmaCSF1RGlycolysisHistone lactylationMAPK signaling

Identifiers

PMID42337539
PMCPMC13584290

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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.