Calcium oscillations triggered by cardiotonic steroids

FEBS J. 2013 Nov;280(21):5450-5. doi: 10.1111/febs.12448. Epub 2013 Sep 2.

Abstract

Na(+), K(+)-ATPase (NKA) is well known for its function as an ion pump. Studies during the last decade have revealed an additional role for NKA as a signal transducer. In this brief review, we describe how cardiotonic steroids, which are highly specific NKA ligands, trigger slow Ca(2+) oscillations by promoting the interaction between NKA and the inositol trisphosphate receptor, and how this Ca(2+) signal activates the NF-κB subunit p65 and increases the expression of the antiapoptotic factor Bcl-xL. The potential tissue-protective effects of this signal are discussed.

Keywords: Ca2+ signaling; NF-κB; Na+-K+-ATPase; Src kinase; apoptosis; cardiotonic steroids; inositol trisphosphate receptor; intracellular Ca2+ oscillations; organ development; ouabain.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis*
  • Calcium Signaling / drug effects*
  • Cardiac Glycosides / pharmacology*
  • Humans
  • NF-kappa B / metabolism*
  • Signal Transduction / drug effects*
  • Sodium-Potassium-Exchanging ATPase / metabolism*

Substances

  • Cardiac Glycosides
  • NF-kappa B
  • Sodium-Potassium-Exchanging ATPase