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.