Bronchopulmonary dysplasia (BPD) continues to be one of the most common complications of preterm birth and is characterized histopathologically by impaired lung alveolarization. Extremely preterm born infants remain at high risk for the development of BPD, highlighting a pressing need for continued efforts to understand the pathomechanisms at play in affected infants. This brief review summarizes recent progress in our understanding of the how the development of the newborn lung is stunted, highlighting recent reports on roles for growth factor signaling, oxidative stress, inflammation, the extracellular matrix and proteolysis, non-coding RNA, and fibroblast and epithelial cell plasticity. Additionally, some concerns about modeling BPD in experimental animals are reviewed, as are new developments in the in vitro modeling of pathophysiological processes relevant to impaired lung alveolarization in BPD.
Keywords: Bronchopulmonary dysplasia; alveolarization; hyperoxia; lung development; pathogenesis.
Copyright © 2018. Published by Elsevier Inc.