ABSTRACT
The new bronchopulmonary dysplasia (BPD) is a disorder characterized by a failure of alveolarization. Alveolarization and angiogenesis are closely linked. If we can determine how to improve angiogenesis in the setting of prematurity and hyperoxia-induced lung disease, we may be able to prevent the development of or modulate the severity of BPD. Recently, it has become clear that postnatal vasculogenesis can occur via circulating endothelial precursor cells (EPCs). A better understanding of the origin and regulation of EPCs may lead to new therapies for prevention and treatment of BPD.
