Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel

Biochim Biophys Acta. 2013 May;1827(5):598-611. doi: 10.1016/j.bbabio.2012.12.007. Epub 2013 Jan 2.

Abstract

In recent years, it has become apparent that there exist several roles for respiratory complex II beyond metabolism. These include: (i) succinate signaling, (ii) reactive oxygen species (ROS) generation, (iii) ischemic preconditioning, (iv) various disease states and aging, and (v) a role in the function of the mitochondrial ATP-sensitive K(+) (mKATP) channel. This review will address the involvement of complex II in each of these areas, with a focus on how complex II regulates or may be involved in the assembly of the mKATP. This article is part of a Special Issue entitled: Respiratory complex II: Role in cellular physiology and disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Aging / genetics*
  • Electron Transport Complex II / genetics*
  • Electron Transport Complex II / metabolism
  • Humans
  • Models, Biological
  • Mutation*
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Physiological Phenomena / genetics
  • Potassium Channels / genetics*
  • Potassium Channels / metabolism

Substances

  • Potassium Channels
  • mitochondrial K(ATP) channel
  • respiratory complex II
  • Adenosine Triphosphate
  • Electron Transport Complex II