Evidence map›Paper›PMID 42204013›Full record

ArticleLung2026

Histone Lactylation Enhances Th17 Cell Differentiation Through DPP4 to Promote Epithelial-Mesenchymal Transition in Asthma.

Xinxin Zhong, Yamei Luo, Jiale Su, Yaxi Liang, Kai Ding, Xiaowen He, Bo Xiao, Lixia Hou, Feiqian Xue, Guiming Zhou and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Lung, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

13 authors.

Xinxin Zhong *Department of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Yamei Luo *Department of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Jiale Su *Department of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Yaxi LiangDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Kai DingDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Xiaowen HeDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Bo XiaoDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Lixia HouDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Feiqian XueDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Guiming ZhouDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Feixiang LingDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Yi GouDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Libing MaDepartment of Respiratory and Critical Care Medicine, Center of Respiratory Medicine, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, China. malibing1984@163.com.

Funding

Guangxi Natural Science Foundation 2022GXNSFAA035452National Natural Science Foundation of China 82260008the Bagui Young Top Talents Training Project of Guangxi Zhuang Autonomous Region 2023
6 · The paper itself

Abstract

backgroundThe airway remodeling in asthma is closely associated with the abnormal differentiation of Th17 cells and epithelial-mesenchymal transition (EMT) of bronchial epithelial cells. This study aims to elucidate the regulatory mechanisms of histone lactylation in Th17 cell differentiation and the EMT of bronchial epithelial cells.

methodsAn asthma mouse model was constructed, pathological changes, immune cell subsets, and histone lactylation levels were analyzed. CD4⁺ T cells from normal and asthmatic mice were treated with a glycolysis activator (Nala) or inhibitor (2-deoxy-glucose (2-DG)). ChIP-qPCR and dual-luciferase assay were performed to verify the regulation of DPP4 promoter by H3K18la. DPP4 inhibitor (K579) was used to intervene in Th17 cell differentiation. Finally, bronchial epithelial cells were induced to undergo EMT by TGF-β1, and co-cultured with CD4

resultsThe asthma mouse model showed lung inflammation, airway remodeling, and imbalance in immune cell subsets. H3K18la and DPP4 levels were upregulated, correlating positively with IL-17. Inhibiting glycolysis reduced H3K18la, inhibited Th17 cell differentiation, and decreased IL-17 secretion. H3K18la activated DPP4 transcription by enriching in DPP4 promoter region. K579 blocked Th17 cell differentiation mediated by H3K18la. Additionally, DPP4 significantly promoted the EMT of bronchial epithelial cells by promoting Th17 cell differentiation, as evidenced by downregulation of E-cadherin, upregulation of α-SMA, and changes in cell morphology. This process was partially inhibited by 2-DG treatment.

conclusionsH3K18la promoted Th17 cell differentiation by activating DPP4, thereby driving the EMT of bronchial epithelial cells. Targeting H3K18la-DPP4-Th17 axis may be a potential asthma therapy.

Indexed as

AsthmaCell DifferentiationDipeptidyl Peptidase 4Epithelial-Mesenchymal TransitionHistonesTh17 CellsAirway RemodelingAnimalsBronchiDipeptidyl-Peptidase IV InhibitorsDisease Models, AnimalEpithelial CellsInterleukin-17MiceMice, Inbred BALB CDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDpp4 protein, mouseHistonesInterleukin-17AsthmaDPP4Dronchial epithelial cellsEpithelial-mesenchymal transitionHistone lactylationTh17 cell differentiation

Identifiers

PMID42204013
PMCPMC13216120

What OpenQuestion holds

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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 OpenQuestion graph.