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lüll Poly(ADP-ribose) polymerase activation in the reperfused myocardium Szabo G; Liaudet L; Hagl S; Szabo CCardiovasc Res 2004[Feb]; 61 (3): 471-80The 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.|Animals[MESH]|Cells, Cultured[MESH]|Enzyme Activation[MESH]|Enzyme Inhibitors/therapeutic use[MESH]|Humans[MESH]|Models, Animal[MESH]|Myocardial Ischemia/enzymology[MESH]|Myocardial Reperfusion Injury/*enzymology[MESH]|Myocardium/*enzymology[MESH]|Niacinamide/therapeutic use[MESH]|Poly(ADP-ribose) Polymerase Inhibitors[MESH]|Poly(ADP-ribose) Polymerases/*metabolism[MESH] |