Ya Pan, Xueli Cheng, Feng Tang, Jiang Lan
BPD develops through complex interactions between developmental immaturity and multiple injurious exposures before and after birth. Improved understanding of disease mechanisms and risk stratification may enhance prevention and early intervention, while future research should focus on targeted therapies to improve both short- and long-term outcomes in preterm infants.
INTRODUCTION: Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of prematurity and remains a leading cause of morbidity in extremely preterm infants. Despite advances in neonatal intensive care, BPD continues to be associated with substantial respiratory and neurodevelopmental sequelae. This review summarizes current evidence regarding the pathophysiology, risk factors, and therapeutic strategies for BPD.
METHODS: A comprehensive search of PubMed, Web of Science, and Embase was conducted using the terms "bronchopulmonary dysplasia", "premature infants", "pathophysiology", "risk factors", and "treatment". English-language studies published up to 2025 were screened, and relevant original studies, reviews, and metaanalyses were included for narrative synthesis.
RESULTS: Current evidence indicates that BPD is a multifactorial disorder characterized by impaired alveolarization and pulmonary vascular development resulting from the interaction of prenatal and postnatal injuries. Key pathogenic pathways include oxidative stress, inflammation, dysregulated angiogenesis, and abnormal tissue repair. Prenatal factors such as chorioamnionitis, placental dysfunction, fetal growth restriction, and genetic susceptibility increase vulnerability, while postnatal exposures including oxygen toxicity, mechanical ventilation, infection, and inadequate nutrition further contribute to disease progression. Evidence-based preventive and therapeutic approaches include lung-protective ventilation, early surfactant therapy, caffeine administration, cautious use of postnatal corticosteroids, and optimization of nutritional support. Nevertheless, targeted therapies remain limited.
CONCLUSIONS: BPD develops through complex interactions between developmental immaturity and multiple injurious exposures before and after birth. Improved understanding of disease mechanisms and risk stratification may enhance prevention and early intervention, while future research should focus on targeted therapies to improve both short- and long-term outcomes in preterm infants.