Reactive oxygen species in early and delayed cardiac adaptation

Abstract

This review focuses on the role of reactive oxygen species in the pathogenesis of cardiac adaptation to ischemia. Results from various laboratories including the authors' confirm the assumption that reactive oxygen species can be an integral part of the induction of both early and delayed forms of cardioprotection. There is conclusive evidence that reactive oxygen species may lead to activation of protein kinase C, protein tyrosine kinase, ionic channel openings and activation of transcriptional factors, all of which may translate into cardioprotection. These findings unveil a contradictory yet fascinating concept that oxygen radicals, although well recognized for their toxicity, can, under special circumstances, beneficially alter cell function leading to increased cell tolerance and survival.

Keywords: Ischemic preconditioning; Myocardial protection; Reactive oxygen species.

Figure 1

Possible signalling mechanism of early and delayed cardiac adaptation. B2 Bradykinin 2 receptor; cAMP Cyclic adenosine mono-phosphate; cGMP Cyclic guanidine monophosphate; DAG Diacylglycerol; Gi G-protein; IP3 Inositoltriphosphate; K_ATP ch ATP-dependant K⁺ channel; MAP kinase Mitogen activated protein kinase; NFκB Nuclear transcription factor; PKC Protein kinase C; PLC Phospholipase C; PLD Phospholipase D; PIP2 Phosphoinositolbiphosphate; PTK Protein tyrosine kinase; ROS Reactive oxygen species; TyK Tyrosine kinase