Nitric oxide: a key regulator of myeloid inflammatory cell apoptosis

Cell Death Differ. 2003 Apr;10(4):418-30. doi: 10.1038/sj.cdd.4401152.


Apoptosis of inflammatory cells is a critical event in the resolution of inflammation, as failure to undergo this form of cell death leads to increased tissue damage and exacerbation of the inflammatory response. Many factors are able to influence the rate of apoptosis in neutrophils, eosinophils, monocytes and macrophages. Among these is the signalling molecule nitric oxide (NO), which possesses both anti- and proapoptotic properties, depending on the concentration and flux of NO, and also the source from which NO is derived. This review summarises the differential effects of NO on inflammatory cell apoptosis and outlines potential mechanisms that have been proposed to explain such actions.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Dose-Response Relationship, Drug
  • Humans
  • Inflammation / drug therapy
  • Inflammation / immunology
  • Inflammation / metabolism*
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / metabolism
  • Myeloid Cells / drug effects
  • Myeloid Cells / immunology
  • Myeloid Cells / metabolism*
  • Nitric Oxide / metabolism*
  • Nitric Oxide Donors / pharmacology
  • Nitric Oxide Donors / therapeutic use


  • Inflammation Mediators
  • Nitric Oxide Donors
  • Nitric Oxide