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Updated: Mar 27, 2026

Real-Time, High-Throughput Microscopic Quantification of Human Neutrophil Extracellular Trap Release and Assessing the Pharmacology of Antagonists
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Regulation of Calcium Homeostasis by PIEZO1 Drives NETosis and Fibrosis in Bronchopulmonary Dysplasia

Lei Cao1, Yan Mao2, Chenxia Juan3

  • 1Department of Orthopedics Trauma, Trauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal of Cellular and Molecular Medicine
|March 25, 2026
PubMed

Insights

Bronchopulmonary dysplasia (BPD) in preterm infants involves lung injury. This study identifies PIEZO1 as a key factor in neutrophil extracellular trap (NET) formation, offering a potential therapeutic target for BPD lung damage and fibrosis.

Area of Science:

  • Neonatal Medicine
  • Pulmonology
  • Molecular Biology

Background:

  • Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants, marked by impaired alveolar development and inflammation.
  • Mechanical ventilation can cause ventilator-induced lung injury, contributing to BPD pathogenesis.

Purpose of the Study:

  • To identify key molecular players and pathways involved in BPD pathogenesis using integrated bioinformatic analysis.
  • To investigate the role of identified genes, particularly PIEZO1, in neutrophil extracellular trap (NET) formation and its contribution to BPD-related lung injury and fibrosis.

Main Methods:

  • Integrated bioinformatic analysis of gene expression datasets (GSE108754, GSE39840) to identify differentially expressed genes (DEGs).
  • Functional enrichment analysis and machine learning algorithms (LASSO, SVM-RFE, Random Forest) to identify hub genes.
  • Immune infiltration analysis, experimental validation of NETosis markers, and co-culture systems to assess PIEZO1 function and its impact on lung epithelial cells.

Main Results:

  • 203 DEGs were identified, enriched in cytokine-mediated signaling and inflammatory responses.
  • Three hub genes (IL6, TFRC, PIEZO1) were identified with high diagnostic accuracy for BPD.
  • PIEZO1 overexpression was found to promote NET formation via calcium overload, which was inhibited by verapamil.
  • PIEZO1-induced NETosis was shown to exacerbate pulmonary fibrosis in lung epithelial cells.

Conclusions:

  • PIEZO1 is a critical regulator of NETosis in bronchopulmonary dysplasia.
  • Targeting PIEZO1 may offer a novel therapeutic strategy to mitigate lung injury and fibrosis in BPD.

Keywords:
Bronchopulmonary dysplasiaPIEZO1calcium homeostasisfibrosisneutrophil extracellular traps

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