The MAPK/JNK signalling pathways offers potential therapeutic targets for the prevention of acquired deafness

A. Zine, T. R. Van De Water

Research output: Contribution to journalReview articlepeer-review

50 Scopus citations


The c-Jun N-terminal kinases (JNKs) are also called stress activated protein kinases (SAPKs) and are members of the family of mitogen activated protein kinases (MAPKs). While the functions of the JNKs under physiological conditions are diverse and not completely understood, there is increasing evidence that JNKs are potent effectors of apoptosis of oxidative stress-damaged cells in both the brain and the mammalian inner ear following a trauma. The activation of the inducible transcription factor c-Jun by N-terminal phosphorylation is a central event in JNK-mediated apoptosis of oxidative stress-damaged auditory hair cells following exposure to either acoustic trauma or a toxic level of an aminoglycoside antibiotic and also the apoptosis of auditory neurons as a consequence of a loss of the trophic support provided by the auditory hair cells. In this review, we summarise what is known about the expression and activation of G-proteins, JNKs, c-Jun and c-Fos under oxidative stress conditions within the mammalian cochlea. A particular focus is put on a new peptide conjugate that is a promising protective agent(s) and pharmacological strategies for preventing cochlear damage induced by both acoustic trauma and aminoglycoside ototoxic damage.

Original languageEnglish (US)
Pages (from-to)325-332
Number of pages8
JournalCurrent Drug Targets: CNS and Neurological Disorders
Issue number4
StatePublished - Aug 1 2004


  • Aminoglycoside ototoxicity
  • Apoptosis of hair cells
  • c-Jun N-terminal kinase (JNK)
  • JNK inhibition
  • Noise-induced hearing loss
  • Organ of Corti
  • Otoprotection
  • Peptide conjugate

ASJC Scopus subject areas

  • Pharmacology
  • Neuroscience(all)


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