Targeting NOX enzymes in pulmonary fibrosis

Louise Hecker, Jeff Cheng, Victor J. Thannickal

Research output: Contribution to journalArticle

43 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)2365-2371
Number of pages7
JournalCellular and Molecular Life Sciences
Volume69
Issue number14
DOIs
StatePublished - Jul 2012
Externally publishedYes

Fingerprint

Idiopathic Pulmonary Fibrosis
Pulmonary Fibrosis
NADPH Oxidase
Reactive Oxygen Species
Oxidative Stress
Enzymes
Oxidants
Oxidoreductases
Protein Isoforms
Fibrosis
Genes
Therapeutics

Keywords

  • Fibrosis
  • NADPH oxidase
  • Oxidative stress

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Molecular Medicine
  • Pharmacology
  • Cellular and Molecular Neuroscience

Cite this

Targeting NOX enzymes in pulmonary fibrosis. / Hecker, Louise; Cheng, Jeff; Thannickal, Victor J.

In: Cellular and Molecular Life Sciences, Vol. 69, No. 14, 07.2012, p. 2365-2371.

Research output: Contribution to journalArticle

Hecker, Louise ; Cheng, Jeff ; Thannickal, Victor J. / Targeting NOX enzymes in pulmonary fibrosis. In: Cellular and Molecular Life Sciences. 2012 ; Vol. 69, No. 14. pp. 2365-2371.
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