Fig. 1
From: Patho-mechanisms of the origins of bronchopulmonary dysplasia
Exposure to hyperoxia leads to production of reactive oxygen species (ROS) that leads to an exaggerated inflammatory response, and releases cytokines and other molecular mediators. Subsequently, this causes abnormal responses of angiogenic factors, growth factor signaling, abnormal matrix protein formation, mitochondrial dysfunction, cell cycle arrest, and cell death. This, in turn, causes impaired alveolarization and dysregulated vasculature which is pathognomic of bronchopulmonary dysplasia (BPD). BAX, bcl-2 like protein; NADPH: nicotinamide adenine dinucleotide phosphate; TGFβ, transforming growth factor β; CTGF, connective tissue growth factor; PDGF, platelet-derived growth factor; KGF, keratinocyte growth factor; VEGF, vascular endothelial growth factor; Ang-2, angiopoietin 2; Cyt c, cytochrome c; IFNγ, interferon gamma; NF-κB, nuclear factor-kappa B; pkB, protein kinase B