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Bronchopulmonary dysplasia - an overview about pathophysiologic concepts
Sophie Niedermaier1,2, Anne Hilgendorff3,4
1Comprehensive Pneumology Center (CPC), Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich Max-Lebsche-Platz 31, 81377, Munich, Germany. Sophie.Niedermaier@med.uni-muenchen.de.
Insights
Bronchopulmonary dysplasia (BPD) in preterm infants impairs lung development, with lasting adult effects. This review explores BPD
Area of Science:
- Neonatology
- Pulmonology
- Pathophysiology
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants.
- It results from impaired pulmonary development with lifelong consequences.
- Key triggers include infection, oxygen toxicity, and mechanical ventilation.
Purpose of the Study:
- To review the pathophysiology of BPD.
- To explore the interplay of disease mechanisms.
- To discuss the long-term effects on adult lung aging and repair.
Main Methods:
- Literature review of pathophysiologic processes in BPD.
- Analysis of cellular and molecular changes.
- Discussion of growth factor signaling in disease development and repair.
Main Results:
- BPD involves sustained inflammation, extracellular matrix remodeling, and apoptosis.
- Altered growth factor signaling is a key feature.
- These changes impact the pulmonary scaffold and cellular interface.
Conclusions:
- BPD's pathophysiology involves complex interactions affecting lung development.
- Long-term consequences include altered adult lung aging and repair processes.
- Understanding these mechanisms is crucial for managing BPD's lifelong impact.
Abstract:
Neonatal chronic lung disease in the preterm infant, i.e. bronchopulmonary dysplasia (BPD) is characterized by impaired pulmonary development with its effects persisting into adulthood. Triggered in the immature lung by infectious complications, oxygen toxicity and the impact of mechanical ventilation, a sustained inflammatory response, extensive remodeling of the extracellular matrix, increased apoptosis as well as altered growth factor signaling characterize the disease. The current review focuses on selected pathophysiologic processes and their interplay in disease development. Furthermore, the potential of both, acute and long-term changes to the pulmonary scaffold and the cellular interface in concert with dysregulated growth factor signaling to affect aging and repair processes in the adult lung is discussed.
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