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Reciprocal interactions between alveolar progenitor dysfunction and aging promote lung fibrosis
Jiurong Liang1, Guanling Huang1, Xue Liu1
1Department of Medicine and Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, United States.
Elife
|June 14, 2023
Summary
Aging and lung injury synergistically impair type 2 alveolar epithelial cell (AEC2) regeneration, contributing to idiopathic pulmonary fibrosis (IPF). This study reveals AEC2 genomic changes in aging and injury, mirroring IPF pathology.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Aging Research
Background:
- Aging is a primary risk factor for idiopathic pulmonary fibrosis (IPF).
- Type 2 alveolar epithelial cell (AEC2) dysfunction and failed regeneration are key to IPF pathogenesis.
- Mechanisms underlying AEC2 regenerative failure in aging and injury are not fully understood.
Purpose of the Study:
- To investigate genomic changes in AEC2s during aging and lung injury.
- To compare AEC2 responses in mice and humans, including IPF patients.
Main Methods:
- Single-cell RNA sequencing (scRNA-seq) of lung epithelial cells from young/old mice (uninjured/bleomycin-injured) and human IPF/healthy donor lungs.
- Analysis of AEC2 subsets, gene expression, and functional correlations.
Main Results:
- Identified three AEC2 subsets; two emerged with aging and injury.
- Aging increased inflammation, stress, senescence, and apoptosis genes in AEC2s.
- Lung injury exacerbated aging-related gene expression in young mice, impairing AEC2 recovery.
- Human IPF AEC2s shared genomic signatures with injured aged mouse AEC2s.
Conclusions:
- Synergistic effects of aging and AEC2 injury drive fibrosis through transcriptomic and functional alterations.
- This research offers novel insights into aging, lung injury, and IPF AEC2 cell interactions.
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