Vijayakumar Karthikeyan A, Cho Gwang-Won, Maharajan Nagarajan, Jang Chul Ho
Department of Biology, College of Natural Science, Chosun University, Gwangju 61452, Korea.
BK21 FOUR Education Research Group for Age-Associated Disorder Control Technology, Department of Integrative Biological Science, Chosun University, Gwangju 61452, Korea.
Exp Neurobiol. 2022 Aug 31;31(4):232-242. doi: 10.5607/en22002.
Tinnitus is the perception of phantom noise without any external auditory sources. The degeneration of the function or activity of the peripheral or central auditory nervous systems is one of the causes of tinnitus. This damage has numerous causes, such as loud noise, aging, and ototoxicity. All these sources excite the cells of the auditory pathway, producing reactive oxygen species that leads to the death of sensory neural hair cells. This causes involuntary movement of the tectorial membrane, resulting in the buzzing noise characteristic of tinnitus. Autophagy is an evolutionarily conserved catabolic scavenging activity inside a cell that has evolved as a cell survival mechanism. Numerous studies have demonstrated the effect of autophagy against oxidative stress, which is one of the reasons for cell excitation. This review compiles several studies that highlight the role of autophagy in protecting sensory neural hair cells against oxidative stress-induced damage. This could facilitate the development of strategies to treat tinnitus by activating autophagy.
耳鸣是在没有任何外部声源的情况下对幻听的感知。外周或中枢听觉神经系统功能或活动的退化是耳鸣的原因之一。这种损伤有多种原因，如噪音、衰老和耳毒性。所有这些因素都会刺激听觉通路的细胞，产生活性氧，导致感觉神经毛细胞死亡。这会导致盖膜的不自主运动，从而产生耳鸣特有的嗡嗡声。自噬是细胞内一种进化保守的分解代谢清除活动，已演变为一种细胞存活机制。大量研究表明自噬对氧化应激有作用，氧化应激是细胞兴奋的原因之一。本综述汇集了多项研究，这些研究突出了自噬在保护感觉神经毛细胞免受氧化应激诱导损伤方面的作用。这可能有助于通过激活自噬来制定治疗耳鸣的策略。
