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Pathophysiology of bronchopulmonary dysplasia (BPD). In the neonatal lung, hyperoxia, ventilation and inflammation contribute to changes in cellular function, leading to blunted repair and persistent distortion in lung architecture. In addition, oxidative-mediated signaling via NF-E2-related factor 2 (Nrf2) results in activation of the pentose phosphate shunt (PPS) with resultant conversion of NADP to NADPH. This provides reducing equivalents to detoxify reactive oxygen species (ROS).
