Poly(ADP-ribosyl)ation and stroke

Pharmacol Res. 2005 Jul;52(1):15-24. doi: 10.1016/j.phrs.2005.02.018.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Ischemia / metabolism
  • Enzyme Inhibitors / pharmacology
  • Enzyme Inhibitors / therapeutic use
  • Glycoside Hydrolases / physiology
  • Humans
  • Neuroprotective Agents / pharmacology
  • Poly (ADP-Ribose) Polymerase-1
  • Poly Adenosine Diphosphate Ribose / metabolism
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Poly(ADP-ribose) Polymerases / physiology*
  • Stroke / drug therapy
  • Stroke / enzymology
  • Stroke / etiology*

Substances

  • Enzyme Inhibitors
  • Neuroprotective Agents
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Poly Adenosine Diphosphate Ribose
  • PARP1 protein, human
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases
  • Glycoside Hydrolases
  • poly ADP-ribose glycohydrolase