Endothelial MLKL Inhibition Reduces Hyperoxia-Induced Bronchopulmonary Dysplasia in Neonatal Mice.

ABSTRACT: Bronchopulmonary dysplasia (BPD) remains a severe complication in premature infants requiring prolonged oxygen therapy, with vascular endothelial dysfunction recognised as a critical contributor to disease progression. Mixed lineage kinase domain-like protein (MLKL)-mediated necroptosis, an essential form of regulated cell death implicated in various pulmonary disorders, has not been fully investigated in the context of BPD. Here, we utilised a neonatal mouse model of hyperoxia exposure to elucidate the role and mechanisms of MLKL-mediated necroptosis in BPD pathogenesis. Our analysis demonstrated morphological characteristics of necroptosis in pulmonary vascular endothelial cells (ECs) under hyperoxic conditions, accompanied by significant elevation of MLKL protein levels and marked upreg

SUBMITTER: Ning J 

PROVIDER: S-EPMC12853218 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature