Cardioprotective effects of poly(ADP-ribose) polymerase inhibition

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

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
Volume52
Issue number1 SPEC. ISS.
DOIs
StatePublished - Jul 2005
Externally publishedYes

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Poly(ADP-ribose) Polymerases
Cardiac Myocytes
Muscle Cells
Reperfusion Injury
Cardiomyopathies
Oxidants
NAD
Adenosine Diphosphate
Reperfusion
Free Radicals
Rodentia
Ischemia
Animal Models
Heart Failure
Cell Culture Techniques
DNA
Wounds and Injuries
Enzymes
Pharmaceutical Preparations
Proteins

Keywords

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

ASJC Scopus subject areas

  • Pharmacology

Cite this

Cardioprotective effects of poly(ADP-ribose) polymerase inhibition. / Szabo, Csaba.

In: Pharmacological Research, Vol. 52, No. 1 SPEC. ISS., 07.2005, p. 34-43.

Research output: Contribution to journalArticle

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