In this study, we established in vivo BPD mouse models and identified that Hdac3 might be an endogenous regulator of BPD, as Hdac3 augmented the abnormal angiogenesis and alveolarization in BPD by enhancing Pgf via the miR-17-EZH1-p65 axis. The gene discussed is PGF; the disease is bronchopulmonary dysplasia.