Nitric oxide: orchestrating hypoxia regulation through mitochondrial respiration and the endoplasmic reticulum stress response

Cell Res. 2005 Jan;15(1):63-5. doi: 10.1038/sj.cr.7290267.

Abstract

Mitochondria have long been considered to be the powerhouse of the living cell, generating energy in the form of the molecule ATP via the process of oxidative phosphorylation. In the past 20 years, it has been recognised that they also play an important role in the implementation of apoptosis, or programmed cell death. More recently it has become evident that mitochondria also participate in the orchestration of cellular defence responses. At physiological concentrations, the gaseous molecule nitric oxide (NO) inhibits the mitochondrial enzyme cytochrome c oxidase (complex IV) in competition with oxygen. This interaction underlies the mitochondrial actions of NO, which range from the physiological regulation of cell respiration, through mitochondrial signalling, to the development of "metabolic hypoxia" -- a situation in which, although oxygen is available, the cell is unable to utilise it.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Calcium / metabolism
  • Cell Respiration
  • Electron Transport Complex IV / metabolism
  • Endoplasmic Reticulum / metabolism*
  • Humans
  • Hypoxia*
  • Mitochondria / metabolism*
  • Nitric Oxide / metabolism*
  • Oxidative Phosphorylation
  • Oxygen / metabolism
  • Oxygen Consumption
  • Phosphorylation
  • Signal Transduction

Substances

  • Nitric Oxide
  • Electron Transport Complex IV
  • Oxygen
  • Calcium