Cardioprotective effects of poly(ADP-ribose) polymerase inhibition

Csaba Szabó

    Research output: Contribution to journalArticlepeer-review

    43 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


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

    ASJC Scopus subject areas

    • Pharmacology


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