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Updated: Mar 18, 2026

Development of a Neonatal Piglet Acute Lung Injury Model Recreating the Early Environment of Preterm Infant Lungs
Published on: October 31, 2025
Early injury of the neonatal lung contributes to premature lung aging: a hypothesis
Silke Meiners1, Anne Hilgendorff2,3
1Comprehensive Pneumology Center (CPC), Ludwig-Maximilians University, Helmholtz Zentrum München, German Center for Lung Research (DZL), Max-Lebsche-Platz 31, 81377, München, Germany. silke.meiners@helmholtz-muenchen.de.
Insights
Bronchopulmonary dysplasia (BPD), a common infant lung disease, may stem from disrupted molecular aging pathways. This could lead to premature lung aging and adult chronic lung disease susceptibility.
Area of Science:
- Neonatal Medicine
- Pulmonology
- Aging Research
Background:
- Bronchopulmonary dysplasia (BPD) is the most frequent chronic lung disease in infancy.
- BPD survivors face long-term pulmonary impairment into adulthood.
- Lung injury from oxygen, ventilation, and infection triggers inflammation and matrix remodeling.
Purpose of the Study:
- To investigate the hypothesis that BPD development involves disturbed molecular aging pathways.
- To explore the link between BPD and premature lung aging.
- To understand increased susceptibility to adult chronic lung diseases.
Main Methods:
- Exploration of conserved molecular aging pathways in the context of BPD.
- Analysis of histopathological characteristics of BPD.
- Review of inflammatory and signaling mechanisms in lung injury.
Main Results:
- BPD is characterized by impaired alveolarization and disrupted vascular development.
- Fibrosis of saccular walls is a key histopathological feature.
- Sustained inflammation and dysregulated growth factor signaling are implicated.
Conclusions:
- Disturbances in molecular aging pathways may contribute to BPD pathogenesis.
- BPD might represent a form of premature lung aging.
- This premature aging could increase adult susceptibility to chronic lung diseases.
Abstract:
Chronic lung disease of the newborn, also known as bronchopulmonary dysplasia (BPD), is the most common chronic lung disease in early infancy and results in an increased risk for long-lasting pulmonary impairment in the adult. BPD develops upon injury of the immature lung by oxygen toxicity, mechanical ventilation, and infections which trigger sustained inflammatory immune responses and extensive remodeling of the extracellular matrix together with dysregulated growth factor signaling. Histopathologically, BPD is characterized by impaired alveolarization, disrupted vascular development, and saccular wall fibrosis. Here, we explore the hypothesis that development of BPD involves disturbance of conserved pathways of molecular aging that may contribute to premature aging of the lung and an increased susceptibility to chronic lung diseases in adulthood.
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