Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss
Mitochondrial dysfunction has been suggested to be a risk factor for sensorineural hearing loss (SNHL) induced by aging, noise, ototoxic drugs, and gene. Reactive oxygen species (ROS) are mainly derived from mitochondria, and oxidative stress induced by ROS contributes to cochlear damage as well as...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2021/5520794 |
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| author | Lingjun Zhang Zhengde Du Shusheng Gong |
| author_facet | Lingjun Zhang Zhengde Du Shusheng Gong |
| author_sort | Lingjun Zhang |
| collection | DOAJ |
| description | Mitochondrial dysfunction has been suggested to be a risk factor for sensorineural hearing loss (SNHL) induced by aging, noise, ototoxic drugs, and gene. Reactive oxygen species (ROS) are mainly derived from mitochondria, and oxidative stress induced by ROS contributes to cochlear damage as well as mitochondrial DNA mutations, which may enhance the sensitivity and severity of hearing loss and disrupt ion homeostasis (e.g., Ca2+ homeostasis). The formation and accumulation of ROS further undermine mitochondrial components and ultimately lead to apoptosis and necrosis. SIRT3–5, located in mitochondria, belong to the family of sirtuins, which are highly conserved deacetylases dependent on nicotinamide adenine dinucleotide (NAD+). These deacetylases regulate diverse cellular biochemical activities. Recent studies have revealed that mitochondrial sirtuins, especially SIRT3, modulate ROS levels in hearing loss pathologies. Although the precise functions of SIRT4 and SIRT5 in the cochlea remain unclear, the molecular mechanisms in other tissues indicate a potential protective effect against hearing loss. In this review, we summarize the current knowledge regarding the role of mitochondrial dysfunction in hearing loss, discuss possible functional links between mitochondrial sirtuins and SNHL, and propose a perspective that SIRT3–5 have a positive effect on SNHL. |
| format | Article |
| id | doaj-art-82dce40759964d4298e504f702ddf6b5 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-82dce40759964d4298e504f702ddf6b52025-02-03T05:52:39ZengWileyNeural Plasticity2090-59041687-54432021-01-01202110.1155/2021/55207945520794Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing LossLingjun Zhang0Zhengde Du1Shusheng Gong2Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing 100050, ChinaDepartment of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing 100050, ChinaDepartment of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing 100050, ChinaMitochondrial dysfunction has been suggested to be a risk factor for sensorineural hearing loss (SNHL) induced by aging, noise, ototoxic drugs, and gene. Reactive oxygen species (ROS) are mainly derived from mitochondria, and oxidative stress induced by ROS contributes to cochlear damage as well as mitochondrial DNA mutations, which may enhance the sensitivity and severity of hearing loss and disrupt ion homeostasis (e.g., Ca2+ homeostasis). The formation and accumulation of ROS further undermine mitochondrial components and ultimately lead to apoptosis and necrosis. SIRT3–5, located in mitochondria, belong to the family of sirtuins, which are highly conserved deacetylases dependent on nicotinamide adenine dinucleotide (NAD+). These deacetylases regulate diverse cellular biochemical activities. Recent studies have revealed that mitochondrial sirtuins, especially SIRT3, modulate ROS levels in hearing loss pathologies. Although the precise functions of SIRT4 and SIRT5 in the cochlea remain unclear, the molecular mechanisms in other tissues indicate a potential protective effect against hearing loss. In this review, we summarize the current knowledge regarding the role of mitochondrial dysfunction in hearing loss, discuss possible functional links between mitochondrial sirtuins and SNHL, and propose a perspective that SIRT3–5 have a positive effect on SNHL.http://dx.doi.org/10.1155/2021/5520794 |
| spellingShingle | Lingjun Zhang Zhengde Du Shusheng Gong Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss Neural Plasticity |
| title | Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss |
| title_full | Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss |
| title_fullStr | Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss |
| title_full_unstemmed | Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss |
| title_short | Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss |
| title_sort | mitochondrial dysfunction and sirtuins important targets in hearing loss |
| url | http://dx.doi.org/10.1155/2021/5520794 |
| work_keys_str_mv | AT lingjunzhang mitochondrialdysfunctionandsirtuinsimportanttargetsinhearingloss AT zhengdedu mitochondrialdysfunctionandsirtuinsimportanttargetsinhearingloss AT shushenggong mitochondrialdysfunctionandsirtuinsimportanttargetsinhearingloss |