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Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss
Reactive oxygen species (ROS) production is involved in several apoptotic and necrotic cell death pathways in auditory tissues. These pathways are the major causes of most types of sensorineural hearing loss, including age-related hearing loss, hereditary hearing loss, ototoxic drug-induced hearing...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385658/ https://www.ncbi.nlm.nih.gov/pubmed/25874222 http://dx.doi.org/10.1155/2015/617207 |
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author | Kamogashira, Teru Fujimoto, Chisato Yamasoba, Tatsuya |
author_facet | Kamogashira, Teru Fujimoto, Chisato Yamasoba, Tatsuya |
author_sort | Kamogashira, Teru |
collection | PubMed |
description | Reactive oxygen species (ROS) production is involved in several apoptotic and necrotic cell death pathways in auditory tissues. These pathways are the major causes of most types of sensorineural hearing loss, including age-related hearing loss, hereditary hearing loss, ototoxic drug-induced hearing loss, and noise-induced hearing loss. ROS production can be triggered by dysfunctional mitochondrial oxidative phosphorylation and increases or decreases in ROS-related enzymes. Although apoptotic cell death pathways are mostly activated by ROS production, there are other pathways involved in hearing loss that do not depend on ROS production. Further studies of other pathways, such as endoplasmic reticulum stress and necrotic cell death, are required. |
format | Online Article Text |
id | pubmed-4385658 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-43856582015-04-13 Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss Kamogashira, Teru Fujimoto, Chisato Yamasoba, Tatsuya Biomed Res Int Review Article Reactive oxygen species (ROS) production is involved in several apoptotic and necrotic cell death pathways in auditory tissues. These pathways are the major causes of most types of sensorineural hearing loss, including age-related hearing loss, hereditary hearing loss, ototoxic drug-induced hearing loss, and noise-induced hearing loss. ROS production can be triggered by dysfunctional mitochondrial oxidative phosphorylation and increases or decreases in ROS-related enzymes. Although apoptotic cell death pathways are mostly activated by ROS production, there are other pathways involved in hearing loss that do not depend on ROS production. Further studies of other pathways, such as endoplasmic reticulum stress and necrotic cell death, are required. Hindawi Publishing Corporation 2015 2015-03-22 /pmc/articles/PMC4385658/ /pubmed/25874222 http://dx.doi.org/10.1155/2015/617207 Text en Copyright © 2015 Teru Kamogashira et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Kamogashira, Teru Fujimoto, Chisato Yamasoba, Tatsuya Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss |
title | Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss |
title_full | Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss |
title_fullStr | Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss |
title_full_unstemmed | Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss |
title_short | Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss |
title_sort | reactive oxygen species, apoptosis, and mitochondrial dysfunction in hearing loss |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385658/ https://www.ncbi.nlm.nih.gov/pubmed/25874222 http://dx.doi.org/10.1155/2015/617207 |
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