P53 maintains lineage fidelity during lung capillary injury-repair in neonatal hyperoxia.

ABSTRACT: 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. Single-cell RNA-Seq identified the activation of numerous p53 target genes in endothelial cells (ECs), including Cdkn1a (p21). While global deletion of p53 resulted in worsened vasculature, EC-specific deletion of p53 reversed the vascular phenotype and improved alveolar simpli

SUBMITTER: Vila Ellis L 

PROVIDER: S-EPMC12487676 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature