Targeting NOX enzymes in pulmonary fibrosis

Cell Mol Life Sci. 2012 Jul;69(14):2365-71. doi: 10.1007/s00018-012-1012-7. Epub 2012 May 23.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Enzyme Inhibitors / pharmacology
  • Enzyme Inhibitors / therapeutic use
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism
  • Humans
  • NADPH Oxidases / antagonists & inhibitors
  • NADPH Oxidases / metabolism*
  • Oxidative Stress
  • Protein Isoforms / antagonists & inhibitors
  • Protein Isoforms / metabolism
  • Pulmonary Fibrosis / enzymology*
  • Pulmonary Fibrosis / pathology
  • Pulmonary Fibrosis / therapy
  • Reactive Oxygen Species / metabolism


  • Enzyme Inhibitors
  • Protein Isoforms
  • Reactive Oxygen Species
  • NADPH Oxidases