p53 maintains lineage fidelity during lung capillary injury-repair in neonatal hyperoxia.

Bronchopulmonary dysplasia (BPD), a prevalent and chronic lung disease affecting premature newborns, results in vascular rarefaction and alveolar simplification. Although the vasculature has been recognized as a main player in this disease, the recently found capillary heterogeneity and cellular dynamics of endothelial subpopulations in BPD remain unclear. Here, we showed that Cap2 cells were damaged during neonatal hyperoxic injury, leading to their replacement by Cap1 cells, which, in turn, significantly declined.

Endothelial deletion of generates transitional endothelial cells and improves lung development during neonatal hyperoxia.

Bronchopulmonary dysplasia (BPD), a prevalent and chronic lung disease affecting premature newborns, results in vascular rarefaction and alveolar simplification. Although the vasculature has been recognized as a main player in this disease, the recently found capillary heterogeneity and cellular dynamics of endothelial subpopulations in BPD remain unclear. Here, we show Cap2 cells are damaged during neonatal hyperoxic injury, leading to their replacement by Cap1 cells which, in turn, significantly decline.