Oxidative stresses and mitochondrial dysfunction in age-related hearing loss.

Oxidative stresses and mitochondrial dysfunction in age-related hearing loss.
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DOI:
10.1155/2014/582849
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发表时间:
2014
影响因子:
--
通讯作者:
Yamasoba T
Yamasoba T
中科院分区:
生物学2区
文献类型:
--
作者:
Fujimoto C;Yamasoba T

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年龄相关性听力损失(ARHL)是老年人群中最常见的感觉障碍,是与衰老相关的进行性听力损失。ARHL的病理包括Corti器、血管纹、传入螺旋神经节神经元以及中枢听觉通路的毛细胞。许多研究表明,线粒体DNA损伤的积累、活性氧的产生和抗氧化功能的降低与随后的耳蜗因应激而发生的衰老有关。线粒体在诱导内源性耳蜗细胞凋亡中起着至关重要的作用。在实验动物中,ARHL可以通过某些干预措施来预防,例如限制热量摄入和补充抗氧化剂。在这篇综述中,我们将重点介绍氧化应激和线粒体功能障碍在动物模型和人类ARHL病理中的作用的研究,并介绍最近出现的关于ARHL发生机制的概念。
Age-related hearing loss (ARHL), the progressive loss of hearing associated with aging, is the most common sensory disorder in the elderly population. The pathology of ARHL includes the hair cells of the organ of Corti, stria vascularis, and afferent spiral ganglion neurons as well as the central auditory pathways. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Mitochondria play a crucial role in the induction of intrinsic apoptosis in cochlear cells. ARHL can be prevented in laboratory animals by certain interventions, such as caloric restriction and supplementation with antioxidants. In this review, we will focus on previous research concerning the role of the oxidative stress and mitochondrial dysfunction in the pathology of ARHL in both animal models and humans and introduce concepts that have recently emerged regarding the mechanisms of the development of ARHL.
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