Abstract
Over the past decade, poly(ADP-ribosyl)ation has emerged as a crucial event in the pathogenesis of ischemic stroke. A large body of evidence unambiguously demonstrates that activity of poly(ADP-ribose) polymerase-1 (PARP-1) significantly increases during brain ischemia, and that inhibition of this enzymatic activity affords substantial neuroprotection from ischemic brain injury. This review strictly focuses on literature on poly(ADP-ribosyl)ation and ischemic stroke, highlighting the pathogenetic role of poly(ADP-ribose) in ischemic neuronal death, and the therapeutic relevance of drugs modulating its metabolism to pharmacological treatment of cerebral ischemia.
MeSH terms
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Animals
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Brain Ischemia / metabolism
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use
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Glycoside Hydrolases / physiology
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Humans
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Neuroprotective Agents / pharmacology
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Poly (ADP-Ribose) Polymerase-1
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Poly Adenosine Diphosphate Ribose / metabolism
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Poly(ADP-ribose) Polymerase Inhibitors
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Poly(ADP-ribose) Polymerases / physiology*
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Stroke / drug therapy
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Stroke / enzymology
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Stroke / etiology*
Substances
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Enzyme Inhibitors
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Neuroprotective Agents
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Poly(ADP-ribose) Polymerase Inhibitors
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Poly Adenosine Diphosphate Ribose
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PARP1 protein, human
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Poly (ADP-Ribose) Polymerase-1
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Poly(ADP-ribose) Polymerases
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Glycoside Hydrolases
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poly ADP-ribose glycohydrolase