Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.

ABSTRACT:

Introduction

Administering high levels of oxygen is a life-sustaining measure in critically ill lung subjects. However, prolonged hyperoxia exposure increases reactive oxygen species (ROS) that exacerbate oxidative stress, mitochondrial dysfunction, respiratory failure, and cell death. Mitochondria play a critical role in hyperoxia-induced acute lung injury (HALI). The specific role of the Polycomb Repressive Complex 1 protein BMI1 (B cell-specific Moloney murine leukemia virus integration site 1) in mitochondrial damage remains unknown.

Methods

Bmi1 knockout mice (Bmi1 ^-/-) and their wild-type (WT) littermates were exposed to normobaric hyperoxia using oxygen concentrations of 95-100% for 48 h to assess BMI1 function in HALI. This research in

SUBMITTER: Hernandez-Cuervo H 

PROVIDER: S-EPMC12658778 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature