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  9. Air Pollution Modelling And Control
  11. H3k18 Lactylation-mediated Six1 Upregulation Contributes To Silica-induced Epithelial-mesenchymal Transition In Airway Epithelial Cells

H3K18 lactylation-mediated SIX1 upregulation contributes to silica-induced epithelial-mesenchymal transition in airway epithelial cells

Songtao Liu1, Yiting He1, Linling Jin1

  • 1Department of Respiratory & Critical Care Medicine, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu 210000, China.

Toxicology
|March 6, 2025

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View abstract on PubMed

Summary
This summary is machine-generated.

Silica exposure triggers airway cell changes (EMT) linked to pulmonary fibrosis. This study reveals an inflammation-glycolysis-lactylation pathway driving EMT, offering new therapeutic targets for lung fibrosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pathology

Background:

  • Airway epithelial-mesenchymal transition (EMT) is a key process in pulmonary fibrosis.
  • Silica exposure is a known cause of lung fibrosis.

Purpose of the Study:

  • To investigate the roles of NLRP3 inflammasome, glycolysis, and histone lactylation in silica-induced EMT.
  • To elucidate the molecular mechanisms linking these factors in human bronchial epithelial cells.

Main Methods:

  • Utilized human bronchial epithelial cells (16HBE) exposed to silica.
  • Employed selective inhibitors for NLRP3 inflammasome (MCC950), IL-1 receptor (AF12198), and lactate production (oxamate).
  • Performed Cut&Tag analysis to assess histone lactylation enrichment.

Main Results:

Keywords:
Epithelial-mesenchymal transition (EMT)GlycolysisHistone lactylationNLRP3 inflammasome

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  • Silica exposure activated NLRP3 inflammasome, enhanced glycolysis and H3K18 lactylation, and induced EMT.
  • Inhibiting NLRP3 inflammasome or IL-1 receptor signaling reduced glycolysis and EMT.
  • Silica-induced H3K18 lactylation at transcription start sites promoted SIX1 expression, driving EMT.

Conclusions:

  • Silica exposure initiates an inflammation-glycolysis-lactylation cascade that promotes EMT.
  • This pathway involves NLRP3 inflammasome activation, IL-1β signaling, PFKFB3-mediated glycolysis, and H3K18 lactylation.
  • Targeting this cascade offers potential therapeutic strategies for silica-induced pulmonary fibrosis.
SIX1
Silica