Reactive oxygen species in early and delayed cardiac adaptation

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.