Abstract
Bronchopulmonary dysplasia (BPD) is a common chronic lung disease in premature infants. Accumulating evidence shows that dysregulated metabolism of glucose, lipids and amino acids are observed in premature infants. Animal and cell studies demonstrate that abnormal metabolism of these substrates results in apoptosis, inflammation, reduced migration, abnormal proliferation or senescence in response to hyperoxic exposure, and that rectifying metabolic dysfunction attenuates neonatal hyperoxia-induced alveolar simplification and vascular dysgenesis in the lung. BPD is often associated with several comorbidities, including pulmonary hypertension and neurodevelopmental abnormalities, which significantly increase the morbidity and mortality of this disease. Here, we discuss recent progress on dysregulated metabolism of glucose, lipids and amino acids in premature infants with BPD and in related in vivo and in vitro models. These findings suggest that metabolic dysregulation may serve as a biomarker of BPD and plays important roles in the pathogenesis of this disease. We also highlight that targeting metabolic pathways could be employed in the prevention and treatment of BPD.