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The Antioxidative Role of Autophagy in Hearing Loss

Autophagy, a highly conserved cellular mechanism, plays an essential role in the development and pathology of many central and peripheral nervous system diseases. The auditory system, especially hair cells (HCs) and spiral ganglion neurons (SGNs) in the inner ear, are postmitotic cells, which are ex...

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Autores principales: Ye, Bin, Fan, Cui, Shen, Yilin, Wang, Quan, Hu, Haixia, Xiang, Mingliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333736/
https://www.ncbi.nlm.nih.gov/pubmed/30686976
http://dx.doi.org/10.3389/fnins.2018.01010
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author Ye, Bin
Fan, Cui
Shen, Yilin
Wang, Quan
Hu, Haixia
Xiang, Mingliang
author_facet Ye, Bin
Fan, Cui
Shen, Yilin
Wang, Quan
Hu, Haixia
Xiang, Mingliang
author_sort Ye, Bin
collection PubMed
description Autophagy, a highly conserved cellular mechanism, plays an essential role in the development and pathology of many central and peripheral nervous system diseases. The auditory system, especially hair cells (HCs) and spiral ganglion neurons (SGNs) in the inner ear, are postmitotic cells, which are extremely reliant on cellular homeostasis and energy supply. Therefore, autophagy may be involved in contributing to and facilitating the normal function of inner ear cells. Recently, studies on hearing loss induced by ototoxic drugs, noise exposure and other factors have revealed that autophagy could serve in an antioxidative capacity and could possess the potential to treat sensorineural hearing loss (SNHL). Therefore, here we review previous studies concerning autophagy and SNHL to gain insight into the role of autophagic mechanisms in inner ear disorders.
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spelling pubmed-63337362019-01-25 The Antioxidative Role of Autophagy in Hearing Loss Ye, Bin Fan, Cui Shen, Yilin Wang, Quan Hu, Haixia Xiang, Mingliang Front Neurosci Neuroscience Autophagy, a highly conserved cellular mechanism, plays an essential role in the development and pathology of many central and peripheral nervous system diseases. The auditory system, especially hair cells (HCs) and spiral ganglion neurons (SGNs) in the inner ear, are postmitotic cells, which are extremely reliant on cellular homeostasis and energy supply. Therefore, autophagy may be involved in contributing to and facilitating the normal function of inner ear cells. Recently, studies on hearing loss induced by ototoxic drugs, noise exposure and other factors have revealed that autophagy could serve in an antioxidative capacity and could possess the potential to treat sensorineural hearing loss (SNHL). Therefore, here we review previous studies concerning autophagy and SNHL to gain insight into the role of autophagic mechanisms in inner ear disorders. Frontiers Media S.A. 2019-01-09 /pmc/articles/PMC6333736/ /pubmed/30686976 http://dx.doi.org/10.3389/fnins.2018.01010 Text en Copyright © 2019 Ye, Fan, Shen, Wang, Hu and Xiang. 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 or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) 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
Ye, Bin
Fan, Cui
Shen, Yilin
Wang, Quan
Hu, Haixia
Xiang, Mingliang
The Antioxidative Role of Autophagy in Hearing Loss
title The Antioxidative Role of Autophagy in Hearing Loss
title_full The Antioxidative Role of Autophagy in Hearing Loss
title_fullStr The Antioxidative Role of Autophagy in Hearing Loss
title_full_unstemmed The Antioxidative Role of Autophagy in Hearing Loss
title_short The Antioxidative Role of Autophagy in Hearing Loss
title_sort antioxidative role of autophagy in hearing loss
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333736/
https://www.ncbi.nlm.nih.gov/pubmed/30686976
http://dx.doi.org/10.3389/fnins.2018.01010
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