Reactive oxygen species, apoptosis, and mitochondrial dysfunction in hearing loss.
Reactive oxygen species, apoptosis, and mitochondrial dysfunction in hearing loss.
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DOI：
10.1155/2015/617207
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发表时间：
2015
影响因子：
--
通讯作者：
Yamasoba T
中科院分区：
文献类型：
--
作者：
Kamogashira T;Fujimoto C;Yamasoba T
活性氧（ROS）的产生参与听觉组织中几种细胞凋亡和坏死的死亡途径。这些途径是大多数类型的感音神经性听力损失的主要原因，包括年龄相关性听力损失、遗传性听力损失、耳毒性药物诱导的听力损失以及噪声诱导的听力损失。ROS的产生可由线粒体氧化磷酸化功能障碍以及ROS相关酶的增加或减少所触发。尽管细胞凋亡死亡途径大多由ROS产生所激活，但还有其他一些与听力损失有关的途径并不依赖于ROS的产生。还需要对其他途径，如内质网应激和细胞坏死进行进一步研究。
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.
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