SOD2
SIRT3
锡尔图因
毛细胞
超氧化物歧化酶
活性氧
细胞生物学
氧化应激
线粒体
噪声性听力损失
线粒体ROS
超氧化物
化学
生物
生物化学
听力损失
医学
内耳
解剖
酶
噪声暴露
听力学
NAD+激酶
作者
Wenqi Liang,Chunli Zhao,Zhong-Rui Chen,Yɑnɡ Zhan,Ke Liu,Shusheng Gong
标识
DOI:10.3389/fcell.2021.766512
摘要
Mitochondrial oxidative stress is involved in hair cell damage caused by noise-induced hearing loss (NIHL). Sirtuin-3 (SIRT3) plays an important role in hair cell survival by regulating mitochondrial function; however, the role of SIRT3 in NIHL is unknown. In this study, we used 3-TYP to inhibit SIRT3 and found that this inhibition aggravated oxidative damage in the hair cells of mice with NIHL. Moreover, 3-TYP reduced the enzymatic activity and deacetylation levels of superoxide dismutase 2 (SOD2). Subsequently, we administered adeno-associated virus-SIRT3 to the posterior semicircular canals and found that SIRT3 overexpression significantly attenuated hair cell injury and that this protective effect of SIRT3 could be blocked by 2-methoxyestradiol, a SOD2 inhibitor. These findings suggest that insufficient SIRT3/SOD2 signaling leads to mitochondrial oxidative damage resulting in hair cell injury in NIHL. Thus, ameliorating noise-induced mitochondrial redox imbalance by intervening in the SIRT3/SOD2 signaling pathway may be a new therapeutic target for hair cell injury.
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