Reactive oxygen species (ROS) are redox-signaling molecules that are critically involved in regulating endothelial cell functions, host defense, aging, and cellular adaptation. Mitochondria are the major sources of ROS and important sources of redox signaling in pulmonary circulation. It is becoming increasingly evident that increased mitochondrial oxidative stress and aberrant signaling through redox-sensitive pathways play a direct causative role in the pathogenesis of many cardiopulmonary disorders including persistent pulmonary hypertension of the newborn (PPHN). This chapter highlights redox signaling in endothelial cells, antioxidant defense mechanism, cell responses to oxidative stress, and their contributions to disease pathogenesis.
Keywords: Asymmetric dimethyl arginine; Extra corporal membrane oxygenation; GTP cyclohydrolase 1; Heat shock protein; Hypoxic inducible factor; Kelch-like ECH-associated protein 1; NADPH oxidase; Nitric oxide synthase; Nuclear factor erythroid 2-related factor 2; Peroxylnitrite ONOO−; Persistent pulmonary hypertension of the newborn; Phosphodiesterase; Phosphoinositol-3 kinase; Protein kinase B; Reactive oxygen species; Superoxide dismutase; Superoxide-O2; Tetrahydrobiopterin.