FIG. 3.

NOX/ROS play a role in the development and regulation of airway diseases. Through activation of redox-sensitive transcription factors and pro-inflammatory gene expression, NOX-derived ROS initiate inflammatory responses in the airways. A correlation between ROS formation and protein kinase C (PKC) activation might play an important role in regulating inflammatory gene transcription. Uncontrolled inflammation, in turn, intensifies ROS generation; thus, NADPH oxidases, as ROS sources, seem to be pivotal therapeutic targets (90)—modified. Some of the currently studied NOX inhibitors have shown promising effects in human settings (in vitro or in vivo) or in animal models of airway diseases. AP-1, activator protein 1; HIF-1α, hypoxia-inducible factor 1-alpha; VCAM-1, vascular cell adhesion molecule-1; cPLA₂, cytosolic phospholipase A₂; ICAM-1, intercellular adhesion molecule-1, MMP-9, matrix metalloproteinase-9; COX-2, cyclooxygenase-2; COPD, chronic obstructive pulmonary disease; ARDS, acute respiratory distress syndrome. Refer to text for further details.