c-Jun N-Terminal Kinases and Their Pharmacological Modulation in Ischemic and Reperfusion Brain Injury

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1 Citation (Scopus)

Abstract

We present here a review of the literature on the role of c-Jun N-terminal kinases (JNK) and their inhibitors in ischemic and reperfusion brain injuries. The functions of JNK in the signal mechanisms involved in brain damage in ischemia and reperfusion are discussed. Effects linked with inhibition of JNK with synthetic and natural compounds in experimental models of ischemia and reperfusion brain injury are described. Results from experimental studies show that JNK provide potential therapeutic targets for protecting the brain from ischemic stroke. However, the fact that JNK have numerous physiological functions prevents systematic use of nonspecific inhibitors of these kinases for therapeutic purposes. The authors conclude that this task requires a further search for selective JNK3 inhibitors.

Original languageEnglish
Pages (from-to)721-728
Number of pages8
JournalNeuroscience and Behavioral Physiology
Volume48
Issue number6
DOIs
Publication statusPublished - 1 Jul 2018

Fingerprint

JNK Mitogen-Activated Protein Kinases
Reperfusion Injury
Brain Injuries
Pharmacology
Brain
Reperfusion
Theoretical Models
Phosphotransferases
Ischemia
Stroke
Therapeutics

Keywords

  • brain
  • c-Jun N-terminal kinase
  • ischemic-reperfusion injury
  • JNK inhibitor
  • stroke
  • therapeutic target

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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abstract = "We present here a review of the literature on the role of c-Jun N-terminal kinases (JNK) and their inhibitors in ischemic and reperfusion brain injuries. The functions of JNK in the signal mechanisms involved in brain damage in ischemia and reperfusion are discussed. Effects linked with inhibition of JNK with synthetic and natural compounds in experimental models of ischemia and reperfusion brain injury are described. Results from experimental studies show that JNK provide potential therapeutic targets for protecting the brain from ischemic stroke. However, the fact that JNK have numerous physiological functions prevents systematic use of nonspecific inhibitors of these kinases for therapeutic purposes. The authors conclude that this task requires a further search for selective JNK3 inhibitors.",
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AB - We present here a review of the literature on the role of c-Jun N-terminal kinases (JNK) and their inhibitors in ischemic and reperfusion brain injuries. The functions of JNK in the signal mechanisms involved in brain damage in ischemia and reperfusion are discussed. Effects linked with inhibition of JNK with synthetic and natural compounds in experimental models of ischemia and reperfusion brain injury are described. Results from experimental studies show that JNK provide potential therapeutic targets for protecting the brain from ischemic stroke. However, the fact that JNK have numerous physiological functions prevents systematic use of nonspecific inhibitors of these kinases for therapeutic purposes. The authors conclude that this task requires a further search for selective JNK3 inhibitors.

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