Excess oxygen may cause lung damage by blocking growth signals and speeding cell aging

Noggin was identified as a hub gene linking bronchopulmonary dysplasia and cellular senescence with an area under the curve (AUC) of 0.80.

• Exposure to 85% hyperoxia resulted in a 2.5-fold increase in Noggin expression and a 50% decrease in BMP4 expression in human pulmonary microvascular endothelial cells.
• Increased expression of p53 and p21, along with positive staining for senescence-associated β-galactosidase, was observed following hyperoxia exposure.
• Silencing of Noggin restored BMP4 levels and reduced hyperoxia-induced upregulation of p53 and p21.
• In a neonatal rat model of hyperoxia-induced bronchopulmonary dysplasia, increased Noggin expression and decreased BMP4 were noted, along with elevated p53 and p21 at day 14.
• These findings indicate that hyperoxia may upregulate Noggin to inhibit BMP4 signaling, which activates cellular senescence pathways and affects alveolar development.

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