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Mechanisms of sensorineural cell damage, death and survival in the cochlea

The majority of acquired hearing loss, including presbycusis, is caused by irreversible damage to the sensorineural tissues of the cochlea. This article reviews the intracellular mechanisms that contribute to sensorineural damage in the cochlea, as well as the survival signaling pathways that can pr...

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Detalles Bibliográficos
Autores principales: Wong, Ann C. Y., Ryan, Allen F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404918/
https://www.ncbi.nlm.nih.gov/pubmed/25954196
http://dx.doi.org/10.3389/fnagi.2015.00058
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author Wong, Ann C. Y.
Ryan, Allen F.
author_facet Wong, Ann C. Y.
Ryan, Allen F.
author_sort Wong, Ann C. Y.
collection PubMed
description The majority of acquired hearing loss, including presbycusis, is caused by irreversible damage to the sensorineural tissues of the cochlea. This article reviews the intracellular mechanisms that contribute to sensorineural damage in the cochlea, as well as the survival signaling pathways that can provide endogenous protection and tissue rescue. These data have primarily been generated in hearing loss not directly related to age. However, there is evidence that similar mechanisms operate in presbycusis. Moreover, accumulation of damage from other causes can contribute to age-related hearing loss (ARHL). Potential therapeutic interventions to balance opposing but interconnected cell damage and survival pathways, such as antioxidants, anti-apoptotics, and pro-inflammatory cytokine inhibitors, are also discussed.
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spelling pubmed-44049182015-05-07 Mechanisms of sensorineural cell damage, death and survival in the cochlea Wong, Ann C. Y. Ryan, Allen F. Front Aging Neurosci Neuroscience The majority of acquired hearing loss, including presbycusis, is caused by irreversible damage to the sensorineural tissues of the cochlea. This article reviews the intracellular mechanisms that contribute to sensorineural damage in the cochlea, as well as the survival signaling pathways that can provide endogenous protection and tissue rescue. These data have primarily been generated in hearing loss not directly related to age. However, there is evidence that similar mechanisms operate in presbycusis. Moreover, accumulation of damage from other causes can contribute to age-related hearing loss (ARHL). Potential therapeutic interventions to balance opposing but interconnected cell damage and survival pathways, such as antioxidants, anti-apoptotics, and pro-inflammatory cytokine inhibitors, are also discussed. Frontiers Media S.A. 2015-04-21 /pmc/articles/PMC4404918/ /pubmed/25954196 http://dx.doi.org/10.3389/fnagi.2015.00058 Text en Copyright © 2015 Wong and Ryan. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Wong, Ann C. Y.
Ryan, Allen F.
Mechanisms of sensorineural cell damage, death and survival in the cochlea
title Mechanisms of sensorineural cell damage, death and survival in the cochlea
title_full Mechanisms of sensorineural cell damage, death and survival in the cochlea
title_fullStr Mechanisms of sensorineural cell damage, death and survival in the cochlea
title_full_unstemmed Mechanisms of sensorineural cell damage, death and survival in the cochlea
title_short Mechanisms of sensorineural cell damage, death and survival in the cochlea
title_sort mechanisms of sensorineural cell damage, death and survival in the cochlea
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404918/
https://www.ncbi.nlm.nih.gov/pubmed/25954196
http://dx.doi.org/10.3389/fnagi.2015.00058
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