Mechanisms of cell death in the injured auditory system: Otoprotective strategies

Philippe P. Lefebvre, Brigitte Malgrange, François Lallemend, Hinrich Staecker, Gustave Moonen, Thomas R. Van De Water

Research output: Contribution to journalArticlepeer-review

80 Scopus citations


Oxidative stress insults such as neurotrophin withdrawal, sound trauma, hypoxia/ischemia, ototoxic antibiotics, and chemotherapeutic agents have been shown to induce apoptosis of both auditory hair cells and neurons. In this paper, we review some components of the apoptotic pathways leading to the death of hair cells and auditory induced by growth factor withdrawal or cisplatin intoxication: (1) reactive oxygen species and free radicals are formed as by-products of several metabolic pathways and these molecules can themselves cause cell damage by reacting with cellular proteins; (2) activation of caspases, and (3) activation of calpain. These mechanisms have several different points at which inhibitors could be targeted to protect cells from programmed cell death, including the prevention of oxidative stress-induced apoptosis and the activation of caspases and calpains.

Original languageEnglish (US)
Pages (from-to)165-170
Number of pages6
JournalAudiology and Neuro-Otology
Issue number3
StatePublished - Jun 22 2002


  • Apoptosis
  • Auditory system
  • Calpain
  • Caspase
  • Cisplatin
  • Reactive oxygen species
  • Trophic factor withdrawal

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Neuroscience(all)
  • Physiology


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