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The injured cochlea as a target for inflammatory processes, initiation of cell death pathways and application of related otoprotectives strategies.

Publication ,  Journal Article
Abi-Hachem, RN; Zine, A; Van De Water, TR
Published in: Recent Pat CNS Drug Discov
June 2010

One of the causes of sensorineural hearing loss is the loss of auditory hair cells following exposure to environmental stresses. Auditory hair cell death in response to cochlear trauma occurs via both necrosis and apoptosis. Apoptosis of hair cells involves the caspase and MAPK/JNK pathways which are activated by oxidative stress and secretion of inflammatory cytokines in response to trauma. Identification of the pathways that lead to apoptosis provides therapeutic targets for the conservation of hearing. Antioxidants reduce the level of reactive oxygen species and reactive nitrogen species generated by oxidative stress in response to acoustic trauma, aminoglycoside and platinum-based drugs. Caspase inhibitors affect both the extrinsic and intrinsic apoptotic pathways thereby reducing cisplatin, aminoglycoside, hydraulic trauma and ischemia-induced hearing losses. Corticosteroid therapy reduces inflammation and inhibits apoptosis while activating pro-survival pathways in the organ of Corti following exposure to noise, vibration, cisplatin, aminoglycoside, ischemia/reperfusion injury, bacterial meningitis and electrode insertion trauma. Inhibitors of JNK signaling pathway prevent apoptosis of auditory hair cells following electrode insertion trauma, acute labyrinthitis, acoustic trauma and aminoglycoside ototoxicity. This review provides an overview of the different pathways involved in auditory hair cell death following an environmental stress and both traditional and newly developed drugs that are currently being studied or used for the treatment of acute hearing loss. Recent patents related to otoprotective strategies to conserve hearing and auditory hair cells are also discussed in this review.

Duke Scholars

Published In

Recent Pat CNS Drug Discov

DOI

EISSN

2212-3954

Publication Date

June 2010

Volume

5

Issue

2

Start / End Page

147 / 163

Location

United Arab Emirates

Related Subject Headings

  • Signal Transduction
  • Neuroprotective Agents
  • Neurology & Neurosurgery
  • Models, Biological
  • MAP Kinase Signaling System
  • JNK Mitogen-Activated Protein Kinases
  • Inflammation
  • Humans
  • Hearing Loss
  • Hair Cells, Auditory
 

Citation

APA
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MLA
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Abi-Hachem, R. N., Zine, A., & Van De Water, T. R. (2010). The injured cochlea as a target for inflammatory processes, initiation of cell death pathways and application of related otoprotectives strategies. Recent Pat CNS Drug Discov, 5(2), 147–163. https://doi.org/10.2174/157488910791213121
Abi-Hachem, Ralph N., Azel Zine, and Thomas R. Van De Water. “The injured cochlea as a target for inflammatory processes, initiation of cell death pathways and application of related otoprotectives strategies.Recent Pat CNS Drug Discov 5, no. 2 (June 2010): 147–63. https://doi.org/10.2174/157488910791213121.
Abi-Hachem, Ralph N., et al. “The injured cochlea as a target for inflammatory processes, initiation of cell death pathways and application of related otoprotectives strategies.Recent Pat CNS Drug Discov, vol. 5, no. 2, June 2010, pp. 147–63. Pubmed, doi:10.2174/157488910791213121.

Published In

Recent Pat CNS Drug Discov

DOI

EISSN

2212-3954

Publication Date

June 2010

Volume

5

Issue

2

Start / End Page

147 / 163

Location

United Arab Emirates

Related Subject Headings

  • Signal Transduction
  • Neuroprotective Agents
  • Neurology & Neurosurgery
  • Models, Biological
  • MAP Kinase Signaling System
  • JNK Mitogen-Activated Protein Kinases
  • Inflammation
  • Humans
  • Hearing Loss
  • Hair Cells, Auditory