Reactive oxygen species in cardiac signalling: from mitochondria to plasma membrane ion channels

Clin Exp Pharmacol Physiol. Jan-Feb 2006;33(1-2):146-51. doi: 10.1111/j.1440-1681.2006.04341.x.

Abstract

1. Reactive oxygen species (ROS) have been considered deleterious to cell function and there is good evidence to suggest that they play a role in the pathophysiology of a number of cardiac disease states. However, ROS are also now being recognized as important regulators of cell function by altering the redox state of proteins. 2. Possible sources of production of ROS in cardiac myocytes are the mitochondria and nicotinamide adenine dinucleotide phosphate-oxidase. The generation of ROS and anti-oxidant defence mechanisms in the heart are discussed. 3. The evidence for a role for ROS in the development of disease states, such as atherosclerosis, ischaemia, cardiac hypertrophy and hypertension, is presented. It is now recognized that cardiac ion channel function is regulated by ROS. Implications with respect to cardiac arrhythmia are discussed.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Membrane / metabolism
  • Heart / physiopathology*
  • Humans
  • Ion Channels / metabolism
  • Mitochondria, Heart / metabolism
  • Models, Biological
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Oxidation-Reduction
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction*

Substances

  • Ion Channels
  • Reactive Oxygen Species