[SIGNALING MECHANISM OF CARDIOPROTECTIVE EFFECT OF REACTIVE OXYGEN SPECIES]

Ross Fiziol Zh Im I M Sechenova. 2015 Apr;101(4):377-85.
[Article in Russian]

Abstract

Protein kinase Cepsilon (PKCepsilon) is a target for reactive oxygen species (ROS). It is activated with reaction products of OH* with phospholipids, which presumably include hydroperoxides of fatty acids or alkylperoxy radicals. Activation of PKCs with reactive oxygen species promotes to mito-K(ATP) channel opening and MPT pore (mitochondrial permeability transition pore) closing thereby it is increasing the resistance of cardiomyocytes to hypoxia-reoxygenation. P38 kinase and tyrosine kinases are targets of ROS. Hydroxyl radical or signaling molecules, resulting from its metabolism, may contribute to the activation of p38-kinase that increases the cardiac tolerance to the impact of ischemia-reperfusion. Src tyrosine kinase and P13-kinase apparently are not targets of ROS. The cardioprotective effect of ROS may be due to the activation of transcription factors NFkappaB and CREB.

Publication types

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

MeSH terms

  • Animals
  • Humans
  • Ischemic Preconditioning, Myocardial*
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / prevention & control*
  • Protein Kinase C-epsilon / metabolism*
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction

Substances

  • Reactive Oxygen Species
  • Protein Kinase C-epsilon