Bronchopulmonary dysplasia (BPD) remains the most common respiratory complication of prematurity as younger and smaller infants are surviving beyond the immediate neonatal period. The recognition that oxidative stress (OS) plays a key role in BPD pathogenesis has been widely accepted since at least the 1980s. In this article, we examine the interplay between OS and genetic regulation and review ‘omics’ data related to OS in BPD. Data from animal models (largely models of hyperoxic lung injury) and from human studies are presented. Epigenetic and transcriptomic analyses have demonstrated several genes related to OS to be differentially expressed in murine models that mimic BPD as well as in premature infants at risk of BPD development and infants with established lung disease. Alterations in the genetic regulation of antioxidant enzymes is a common theme in these studies. Data from metabolomics and proteomics have also demonstrated the potential involvement of OS-related pathways in BPD. A limitation of many studies includes the difficulty of obtaining timely and appropriate samples from human patients. Additional ‘omics’ studies could further our understanding of the role of OS in BPD pathogenesis, which may prove beneficial for prevention and timely diagnosis, and aid in the development of targeted therapies.

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