The mitochondrion: A perpetrator of acquired hearing loss

被引:165
作者
Boettger, Erik C. [1 ]
Schacht, Jochen [2 ]
机构
[1] Univ Zurich, Inst Med Mikrobiol, Zurich, Switzerland
[2] Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
COCHLEAR HAIR-CELLS; DNA COMMON DELETION; DIETARY RESTRICTION; OXIDATIVE STRESS; FREE-RADICALS; INNER-EAR; GENTAMICIN; PATHOLOGY; PRESBYACUSIS; ASSOCIATION;
D O I
10.1016/j.heares.2013.01.006
中图分类号
R36 [病理学]; R76 [耳鼻咽喉科学];
学科分类号
100104 ; 100213 ;
摘要
Age, drugs, and noise are major causes of acquired hearing loss. The involvement of reactive oxygen species (ROS) in hair cell death has long been discussed, but there is considerably less information available as to the mechanisms underlying ROS formation. Most cellular ROS arise in mitochondria and this review will evaluate evidence for mitochondrial pathology in general and dysfunction of the mitochondrial respiratory chain in particular in acquired hearing loss. We will discuss evidence that different pathways can lead to the generation of ROS and that oxidative stress might not necessarily be causal to all three pathologies. Finally, we will detail recent advances in exploiting knowledge of aminoglycoside-mitochondria interactions for the development of non-ototoxic antibacterials. This article is part of a Special Issue entitled "Annual Reviews 2013". (C) 2013 Elsevier B.V. All rights reserved.
引用
收藏
页码:12 / 19
页数:8
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