TGFB1 and bronchopulmonary dysplasia: Beyond oxidative stress, hyperoxia promotes fibrosis in the developing lung, particularly in preterm infants, via ROS-driven inflammation, TGF-β signaling, fibroblast–myofibroblast differentiation, and ECM accumulation, contributing to BPD pathogenesis [31,33,42,119,120,121,122,123,124,125,126,127].