Bronchopulmonary dysplasia (BPD) is the most common morbidity in very preterm infants, and is characterized by abnormal development of the lung. The pathophysiology of BPD is primarily due to effects of placental dysfunction, hyperoxia, ventilator-induced lung injury, poor nutrition, abnormal blood flow, and genomic/epigenomic factors on an immature lung. These adverse factors act on multiple cell types through many interacting signaling pathways. Abnormal development impacts most structures of the lung including the alveoli, blood vessels, and airways, and frequently results in long-term impairment of lung mechanics and function. In this review, we provide a detailed overview of the processes involved in lung development and function and how these pathways are disrupted in BPD. The resulting effects on lung histology and lung mechanics and gas exchange are described. Insights derived from recent molecular and cellular characterization of lungs derived from normal and BPD-affected infants indicate possible mechanisms of pathogenesis and suggest potential new therapeutic strategies. The long-term implications of abnormal lung development as seen in BPD on later childhood and adult life are discussed.
Ambalavanan et al. (2025) studied this question.