Reactive oxygen species and the neuronal fate

Cell Mol Life Sci. 2012 Jan;69(2):215-21. doi: 10.1007/s00018-011-0807-2. Epub 2011 Sep 23.

Abstract

Aberrant or elevated levels of reactive oxygen species (ROS) can mediate deleterious cellular effects, including neuronal toxicity and degeneration observed in the etiology of a number of pathological conditions, including Alzheimer's and Parkinson's diseases. Nevertheless, ROS can be generated in a controlled manner and can regulate redox sensitive transcription factors such as NFκB, AP-1 and NFAT. Moreover, ROS can modulate the redox state of tyrosine phosphorylated proteins, thereby having an impact on many transcriptional networks and signaling cascades important for neurogenesis. A large body of literature links the controlled generation of ROS at low-to-moderate levels with the stimulation of differentiation in certain developmental programs such as neurogenesis. In this regard, ROS are involved in governing the acquisition of the neural fate-from neural induction to the elaboration of axons. Here, we summarize and discuss the growing body of literature that describe a role for ROS signaling in neuronal development.

Publication types

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

MeSH terms

  • Animals
  • Female
  • Humans
  • Male
  • Mice
  • NADPH Oxidases / metabolism
  • Nervous System / growth & development
  • Nervous System / metabolism*
  • Neurogenesis*
  • Neurons / enzymology
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction

Substances

  • Reactive Oxygen Species
  • NADPH Oxidases