Fig. 7From: Involvement of Hdac3-mediated inhibition of microRNA cluster 17-92 in bronchopulmonary dysplasia developmentSchematic diagram depicting the role of Hdac3 regulating the miR-17-EZH1-p65-Pgf axis in BPD in neonatal mice. Hdac3 is highly expressed in lung fibroblasts of BPD mice, inhibiting the expression of miR-17 in the miR-17-92 cluster. In addition, Hdac3 attenuates the binding of miR-17 to EZH1, and consequently upregulates the transcription and expression of Pgf, a downstream target gene of transcription factor p65. This thereby promotes angiogenesis and alveolar formation, and aggravates the progression of BPDBack to article page