FIG. 3.

NOX expression and function in lung fibrosis. NOXs are a source of ROS in alveolar epithelial cells, macrophages, neutrophils, myofibroblasts, endothelial cells, and VSMCs. H₂O₂ and O₂· ⁻ participate in determination of cell phenotype and fate by regulating immune cell recruitment/activation, EMT, myofibroblast differentiation, and ECM remodeling, which may all contribute to the pathogenesis of lung fibrosis. H₂O₂, hydrogen peroxide; Keap1, Kelch-like ECH-associated protein 1; MAPK, mitogen-activated protein kinase; Nrf2, nuclear factor erythroid-derived 2-like 2. Color images are available online.