Molecular mechanisms of hyperoxia-induced acute lung injury

Abstract

Hyperoxia-induced acute lung injury (HALI) is characterized by an influx of inflammatory cells, increased pulmonary permeability, endothelial and epithelial cell death. Reactive oxygen species have been postulated to have a significant role in HALI, in part, by inducing cell death responses regulated by shared common mediators of apoptotic and necrotic pathways. Significant differences exist in the response of the mature and developing lung to HALI.