SR/ER-mitochondrial local communication: calcium and ROS

Biochim Biophys Acta. 2009 Nov;1787(11):1352-62. doi: 10.1016/j.bbabio.2009.06.004. Epub 2009 Jun 13.

Abstract

Mitochondria form junctions with the sarco/endoplasmic reticulum (SR/ER), which support signal transduction and biosynthetic pathways and affect organellar distribution. Recently, these junctions have received attention because of their pivotal role in mediating calcium signal propagation to the mitochondria, which is important for both ATP production and mitochondrial cell death. Many of the SR/ER-mitochondrial calcium transporters and signaling proteins are sensitive to redox regulation and are directly exposed to the reactive oxygen species (ROS) produced in the mitochondria and SR/ER. Although ROS has been emerging as a novel signaling entity, the redox signaling of the SR/ER-mitochondrial interface is yet to be elucidated. We describe here possible mechanisms of the mutual interaction between local Ca(2+) and ROS signaling in the control of SR/ER-mitochondrial function.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Signaling
  • Endoplasmic Reticulum / metabolism*
  • Humans
  • Inositol 1,4,5-Trisphosphate Receptors / physiology
  • Mitochondria / metabolism*
  • Reactive Oxygen Species / metabolism*
  • Ryanodine Receptor Calcium Release Channel / physiology
  • Sarcoplasmic Reticulum / metabolism*
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases / physiology

Substances

  • Inositol 1,4,5-Trisphosphate Receptors
  • Reactive Oxygen Species
  • Ryanodine Receptor Calcium Release Channel
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases
  • ATP2A2 protein, human
  • Calcium