Cardioprotective effects of poly(ADP-ribose) polymerase inhibition

Csaba Szabó

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Free radical and oxidant production in cardiac myocytes during ischemia/reperfusion, cardiomyopathy, cardiotoxic drug exposure and ageing leads to DNA strand-breakage which activates the nuclear enzyme poly(ADP-ribose) polymerase (PARP) and initiates an energy consuming, inefficient cellular metabolic cycle with transfer of the ADP-ribosyl moiety of NAD+ to protein acceptors. These processes lead to the functional impairment of the myocytes and promote myocyte death. During the last decade a growing number of experimental studies demonstrated the beneficial effects of PARP inhibition in cell cultures through rodent models and more recently in pre-clinical large animal models of regional and global ischemia/reperfusion injury and various forms of heart failure. The current article provides an overview of the experimental evidence implicating PARP as a pathophysiological modulator of cardiac myocyte injury in vitro and in vivo.

Original languageEnglish (US)
Pages (from-to)34-43
Number of pages10
JournalPharmacological Research
Issue number1 SPEC. ISS.
StatePublished - Jul 2005
Externally publishedYes


  • Cytokines
  • Heart
  • Myocardial infarction
  • Nitric oxide
  • Oxidative stress
  • Peroxynitrite
  • Poly(ADP-ribose) polymerase
  • Preconditioning

ASJC Scopus subject areas

  • Pharmacology


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