Cellular and Molecular Life Sciences

, Volume 69, Issue 14, pp 2373–2385 | Cite as

NOX enzymes: potential target for the treatment of acute lung injury

  • Stéphanie Carnesecchi
  • Jean-Claude Pache
  • Constance Barazzone-Argiroffo
Multi-author review

Abstract

Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), is characterized by acute inflammation, disruption of the alveolar-capillary barrier, and in the organizing stage by alveolar pneumocytes hyperplasia and extensive lung fibrosis. The cellular and molecular mechanisms leading to the development of ALI/ARDS are not completely understood, but there is evidence that reactive oxygen species (ROS) generated by inflammatory cells as well as epithelial and endothelial cells are responsible for inflammatory response, lung damage, and abnormal repair. Among all ROS-producing enzymes, the members of NADPH oxidases (NOXs), which are widely expressed in different lung cell types, have been shown to participate in cellular processes involved in the maintenance of lung integrity. It is not surprising that change in NOXs’ expression and function is involved in the development of ALI/ARDS. In this context, the use of NOX inhibitors could be a possible therapeutic perspective in the management of this syndrome. In this article, we summarize the current knowledge concerning some cellular aspects of NOXs localization and function in the lungs, consider their contribution in the development of ALI/ARDS and discuss the place of NOX inhibitors as potential therapeutical target.

Keywords

NOX enzymes Acute lung injury Acute respiratory distress syndrome 

Abbreviations

ALI

Acute lung injury

ARDS

Acute respiratory distress syndrome

BAL

Bronchoalveolar lavage

ROS

Reactive oxygen species

HM

Hyaline membranes

LPS

Lipopolysaccharide

TNF-α

Tumor necrosis factor-α

ICAM-1

Intracellular adhesion molecule-1

EC

Endothelial cells

TGF-β1

Transforming growth factor-β1

IPF

Idiopathic pulmonary fibrosis

IRF-3

Interferon regulatory factor-3

AP1

Activator protein 1

NF-κB

Nucleor factor κB

MCP-1

Monocyte chemotactic protein-1

MV

Mechanical ventilation

N.D.

Not determined

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Copyright information

© Springer Basel AG 2012

Authors and Affiliations

  • Stéphanie Carnesecchi
    • 1
  • Jean-Claude Pache
    • 2
  • Constance Barazzone-Argiroffo
    • 1
  1. 1.Department of Pediatrics/Pathology and ImmunologyCentre Médical UniversitaireGenevaSwitzerland
  2. 2.Department of Pathology and ImmunologyCentre Médical UniversitaireGenevaSwitzerland

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