Reactive oxygen species in early and delayed cardiac adaptation

E. Rőth, M. T. Jaberansari

Research output: Contribution to journalArticle

3 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)81-86
Number of pages6
JournalExperimental and Clinical Cardiology
Volume6
Issue number2
Publication statusPublished - 2001

Fingerprint

Reactive Oxygen Species
Ion Channels
Protein-Tyrosine Kinases
Protein Kinase C
Transcriptional Activation
Cell Survival
Ischemia

Keywords

  • Ischemic preconditioning
  • Myocardial protection
  • Reactive oxygen species

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Reactive oxygen species in early and delayed cardiac adaptation. / Rőth, E.; Jaberansari, M. T.

In: Experimental and Clinical Cardiology, Vol. 6, No. 2, 2001, p. 81-86.

Research output: Contribution to journalArticle

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