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Reactive nitrogen species and cell signaling: implications for death or survival of lung epithelium

Yvonne M W Janssen-Heininger1, Rebecca L Persinger, Solange H Korn

  • 1Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont 05405, USA. yjanssen@zoo.uvm.edu

American Journal of Respiratory and Critical Care Medicine
|December 10, 2002
PubMed

Insights

Reactive nitrogen species contribute to inflammatory lung diseases by affecting cell signaling. This review examines nuclear factor kappa B and c-Jun-N-terminal kinase pathways in oxidative stress responses.

Area of Science:

  • Pulmonary Medicine
  • Molecular Biology
  • Cellular Signaling

Background:

  • Reactive nitrogen species (RNS), including nitric oxide, peroxynitrite, and nitrogen dioxide, are linked to inflammatory lung disease pathology.
  • The precise molecular mechanisms driving cellular injury in these conditions are not fully understood.
  • Cell survival and cell death are governed by critical signaling pathways.

Purpose of the Study:

  • To review the roles of nuclear factor kappa B (NF-κB) and c-Jun-N-terminal kinase (JNK) signaling pathways.
  • To elucidate the molecular mechanisms of RNS-induced cellular injury in lung diseases.
  • To discuss the importance of these pathways in oxidative stress responses within lung epithelial cells.

Main Methods:

  • Literature review of signaling pathways.
  • Analysis of molecular mechanisms in cellular injury.
  • Discussion of oxidative stress responses in lung epithelial cells.

Main Results:

  • NF-κB and JNK pathways are key regulators of cell survival and death, respectively.
  • These pathways are intricately involved in the cellular response to oxidative stress.
  • RNS significantly impact these signaling cascades in the context of lung inflammation.

Conclusions:

  • NF-κB and JNK signaling are central to understanding RNS-mediated lung pathophysiology.
  • Further research into these pathways can identify therapeutic targets for inflammatory lung diseases.
  • Elucidating these mechanisms is crucial for managing cellular injury caused by oxidative stress.

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