We did not elucidate the: (1) sex-specific effects of endothelial AMPKα1 deficiency; (2) impact of hyperoxia or endothelial AMPKα1 deficiency on lung function; (3) impact of AMPKα1 activation on hyperoxia-induced experimental BPD-PH; and (4) precise molecular mechanisms through which endothelial AMPKα1 deficiency potentiates neonatal hyperoxic lung injury. Here, PRKAA1 is linked to bronchopulmonary dysplasia.