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Cardiovascular Research 2004 61(3):471-480; doi:10.1016/j.cardiores.2003.09.029
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Poly(ADP-ribose) polymerase activation in the reperfused myocardium

Gábor Szabó*,a, Lucas Liaudetb, Siegfried Hagla and Csaba Szabób,c

aDepartment of Cardiac Surgery, University of Heidelberg, Im Neuenheimer Feld 110, Heidelberg 69120, Germany
bInotek Pharmaceuticals Corporation, Beverly, MA 01915, USA
cInstitute of Human Physiology, Semmelweis University Medical School, Budapest, Hungary

* Corresponding author. Tel.: +49-6221-566111; fax: +49-6221-565585. dzsi{at}hotmail.com

The activation of poly(ADP-ribose) polymerase (PARP) is now considered a final common effector in various types of tissue injury including systemic inflammation, circulatory shock and ischemia/reperfusion. Free radical and oxidant production and related cytotoxicity during ischemia/reperfusion leads to DNA strand breakage which activates the nuclear enzyme PARP and initiates an energy-consuming, inefficient cellular metabolic cycle with transfer of the ADP-ribosyl moiety of NAD+ to protein acceptors. During the last 5 years, 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. The objective of the current review is to provide an overview of the experimental evidence implicating PARP as a pathophysiological modulator of myocardial injury in vitro and in vivo.

KEYWORDS Poly(ADP-ribose) polymerase; Peroxynitrite; Oxidative stress; Reperfusion injury; Heart

Time for primary review 20 days


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