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Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species
A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing lo...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Bentham Science Publishers Ltd.
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923367/ https://www.ncbi.nlm.nih.gov/pubmed/21119884 http://dx.doi.org/10.2174/157015910791233123 |
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author | Tabuchi, Keiji Nishimura, Bungo Tanaka, Shuho Hayashi, Kentaro Hirose, Yuki Hara, Akira |
author_facet | Tabuchi, Keiji Nishimura, Bungo Tanaka, Shuho Hayashi, Kentaro Hirose, Yuki Hara, Akira |
author_sort | Tabuchi, Keiji |
collection | PubMed |
description | A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing loss reportedly arise from ischemic injury, the pathological mechanism of cochlear ischemia-reperfusion injury has not been fully elucidated. Recent animal studies have shed light on the mechanisms of cochlear ischemia-reperfusion injury. It will help in the understanding of the pathology of cochlear ischemia-reperfusion injury to classify this injury into ischemic injury and reperfusion injury. Excitotoxicity, mainly observed during the ischemic period, aggravates the injury of primary auditory neurons. On the other hand, oxidative damage induced by hydroxyl radicals and nitric oxide enhances cochlear reperfusion injury. This article briefly summarizes the generation mechanisms of cochlear ischemia-reperfusion injury and potential therapeutic targets that could be developed for the effective management of this injury type. |
format | Text |
id | pubmed-2923367 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Bentham Science Publishers Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-29233672010-12-01 Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species Tabuchi, Keiji Nishimura, Bungo Tanaka, Shuho Hayashi, Kentaro Hirose, Yuki Hara, Akira Curr Neuropharmacol Article A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing loss reportedly arise from ischemic injury, the pathological mechanism of cochlear ischemia-reperfusion injury has not been fully elucidated. Recent animal studies have shed light on the mechanisms of cochlear ischemia-reperfusion injury. It will help in the understanding of the pathology of cochlear ischemia-reperfusion injury to classify this injury into ischemic injury and reperfusion injury. Excitotoxicity, mainly observed during the ischemic period, aggravates the injury of primary auditory neurons. On the other hand, oxidative damage induced by hydroxyl radicals and nitric oxide enhances cochlear reperfusion injury. This article briefly summarizes the generation mechanisms of cochlear ischemia-reperfusion injury and potential therapeutic targets that could be developed for the effective management of this injury type. Bentham Science Publishers Ltd. 2010-06 /pmc/articles/PMC2923367/ /pubmed/21119884 http://dx.doi.org/10.2174/157015910791233123 Text en ©2010 Bentham Science Publishers Ltd. http://creativecommons.org/licenses/by/2.5/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Article Tabuchi, Keiji Nishimura, Bungo Tanaka, Shuho Hayashi, Kentaro Hirose, Yuki Hara, Akira Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species |
title | Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species |
title_full | Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species |
title_fullStr | Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species |
title_full_unstemmed | Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species |
title_short | Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species |
title_sort | ischemia-reperfusion injury of the cochlea: pharmacological strategies for cochlear protection and implications of glutamate and reactive oxygen species |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923367/ https://www.ncbi.nlm.nih.gov/pubmed/21119884 http://dx.doi.org/10.2174/157015910791233123 |
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