title: Targeting NOX enzymes in pulmonary fibrosis.
abstract: Oxidative stress has been associated with a number of human fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). Oxidative stress is most often defined as an imbalance between the generation of reactive oxygen species (ROS) in excess of the capacity of cells/tissues to detoxify or scavenge them. Additionally, the regulated production of ROS participates in cellular signaling. Therapeutic strategies to treat IPF have, thus far, focused on augmenting anti-oxidant capacity. Recent studies have demonstrated a critical role for ROS-generating enzymatic systems, specifically, NADPH oxidase (NOX) family oxidoreductases in fibrotic processes. In this review, we examine the evidence for NOX isoforms in the generation and perpetuation of fibrosis, and the potential to target this gene family for the treatment of IPF and related fibrotic disorders.
authors.affiliation: Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, 35294-0006, USA. lhecker@uab.edu
authors.forename: Louise
authors.initials: L
authors.lastname: Hecker
authors.forename: Jeff
authors.initials: J
authors.lastname: Cheng
authors.forename: Victor J
authors.initials: VJ
authors.lastname: Thannickal
mesh_terms: D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D018384:Oxidative Stress; D020033:Protein Isoforms / Q000037:antagonists & inhibitors / Q000378:metabolism; D011658:Pulmonary Fibrosis / Q000201:enzymology* / Q000473:pathology / Q000628:therapy; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D020033:Protein Isoforms; D017382:Reactive Oxygen Species; D019255:NADPH Oxidases