Equivocal roles of tissue-type plasminogen activator in stroke-induced injury

Trends Neurosci. 2004 Mar;27(3):155-60. doi: 10.1016/j.tins.2003.12.011.

Abstract

Stroke represents a major health problem in the ever-ageing population of industrialized nations. Each year, over three million people in the USA alone suffer from this affliction. Stroke, which results from the obstruction of an intra- or extra-cerebral artery, induces irreversible neuronal damage. The clot-busting drug tissue-type plasminogen activator (tPA) is the only FDA-approved therapy for acute stroke. Although tPA has been successfully used to treat myocardial infarction due to clot formation, its use in the treatment of occlusive cerebrovascular diseases remains controversial. Indeed, tPA is clearly beneficial as a thrombolytic agent. However, increasing evidence suggests that tPA could have direct and deleterious effects on neurons and glial cells.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Death / drug effects
  • Disease Models, Animal
  • Fibrinolytic Agents / adverse effects
  • Fibrinolytic Agents / therapeutic use*
  • Glutamic Acid / metabolism
  • Humans
  • Neuroglia / drug effects*
  • Neurons / drug effects*
  • Neuroprotective Agents / adverse effects
  • Neuroprotective Agents / therapeutic use
  • Signal Transduction / drug effects
  • Stroke / complications*
  • Stroke / drug therapy*
  • Thrombolytic Therapy / methods
  • Tissue Plasminogen Activator / adverse effects
  • Tissue Plasminogen Activator / therapeutic use*
  • Transforming Growth Factor beta / therapeutic use
  • Transforming Growth Factor beta1

Substances

  • Fibrinolytic Agents
  • Neuroprotective Agents
  • TGFB1 protein, human
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Glutamic Acid
  • Tissue Plasminogen Activator