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Regulation of caspases by nitric oxide

Peter K M Kim1, Young-Guen Kwon, Hun-Taeg Chung

  • 1Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Annals of the New York Academy of Sciences
|June 22, 2002
PubMed

Insights

Nitric oxide

Area of Science:

  • Biochemistry
  • Cell Biology
  • Immunology

Background:

  • Nitric oxide (NO) concentration-dependently modulates apoptosis and inflammation.
  • NO inhibits apoptosis by S-nitrosylation of caspases, key regulators of cell death.
  • NO's effect on caspases is influenced by iron and cellular redox state.

Purpose of the Study:

  • To review the complex relationship between nitric oxide and caspase activity.
  • To explore the role of iron in modulating NO's effects on caspases.
  • To discuss clinical implications for NO in inflammation and apoptosis regulation.

Main Methods:

  • Literature review of studies investigating nitric oxide, caspases, and apoptosis.
  • Analysis of mechanisms of caspase S-nitrosylation by nitric oxide.
  • Examination of indirect pathways through which NO influences caspase activation.

Main Results:

  • Nitric oxide can inhibit or induce apoptosis based on concentration, cell type, and oxidative environment.
  • NO directly inhibits caspases via S-nitrosylation, but can indirectly promote apoptosis.
  • Iron availability and intracellular redox potential are critical for NO's S-nitrosylation of caspases.

Conclusions:

  • Nitric oxide's dual role in apoptosis requires careful consideration of cellular context.
  • Understanding NO-caspase interactions is crucial for therapeutic strategies targeting inflammation and cell death.
  • Iron modulation of NO's effects on caspases presents potential therapeutic targets.

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