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

      Cardiovascular Research

      Cells, Cultured, Enzyme Activation, Enzyme Inhibitors, therapeutic use, Humans, Models, Animal, Myocardial Ischemia, enzymology, Myocardial Reperfusion Injury, metabolism, Myocardium, Niacinamide, Poly(ADP-ribose) Polymerases, antagonists & inhibitors, Animals

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          Abstract

          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.

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          Journal
          14962478
          10.1016/j.cardiores.2003.09.029

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