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Syndecan-1 Promotes Alveolar Type 2 Epithelial Cell Senescence during Lung Fibrosis
Changfu Yao1, Milena Espinola1, Xue Liu1
1Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Biorxiv : the Preprint Server for Biology
|March 27, 2026
Summary
Syndecan-1 is elevated in lung fibrosis, promoting alveolar cell senescence and impairing repair. Reducing syndecan-1 preserves lung epithelial function, suggesting it as a therapeutic target for idiopathic pulmonary fibrosis.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Regenerative Medicine
Background:
- Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease with limited therapies.
- Alveolar type 2 (AT2) cells are crucial for lung repair but dysfunction in IPF.
- Syndecan-1's role in AT2 cell dysfunction in fibrosis is not well understood.
Purpose of the Study:
- Investigate the role of syndecan-1 in AT2 cell dysfunction and lung fibrosis.
- Determine if syndecan-1 is a potential therapeutic target for IPF.
Main Methods:
- Analysis of human IPF tissues and aged mice.
- Murine bleomycin-induced lung fibrosis model.
- Human transcriptomic analysis, genetic mouse models, and epithelial cell systems.
Main Results:
- Syndecan-1 is upregulated in AT2 cells in IPF, aging, and experimental fibrosis.
- Excess syndecan-1 drives AT2 cell senescence and impairs progenitor function.
- Loss of syndecan-1 attenuates senescence and preserves epithelial repair after injury.
Conclusions:
- Syndecan-1 is a key regulator of AT2 cell senescence and maladaptive repair in pulmonary fibrosis.
- Targeting syndecan-1-driven epithelial dysfunction offers a potential therapeutic strategy for IPF.
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