Preterm infants with bronchopulmonary dysplasia (BPD), characterized by pulmonary inflammation leading to impaired alveolarization and vascular dysregulation, have an increased risk of abnormal lung function in infancy, childhood, and adulthood. These include a heightened risk of pulmonary hypertension, and respiratory illnesses. MicroRNAs (miRNAs) are known to disrupt normal lung development and function by interrupting alveolarization and vascularization resulting in the development of BPD. Among the various miRs involved in BPD, miR34a has been shown to have a significant role in BPD pathogenesis. Targeting miR34a or its downstream targets may be a promising therapeutic intervention for BPD. In this review, we summarize the data on cellular arrest, proliferation, differentiation, epithelial-mesenchymal transition, mitochondrial dysfunction, and apoptosis impacted by miR34a in the development of BPD pulmonary phenotypes while predicting the future perspective of miR34a in BPD.
Keywords: arrested alveolarization; bronchopulmonary dysplasia; dysregulated angiogenesis; miR34a; miR34a antagomir.