氧化应激在老年性聋发病机制中的研究进展
Progress of research of oxidative stress in the pathogenesis of presbycusis
周颖东 1张梦娴 1王青玲 1康浩然 2郭向东2
作者信息
- 1. 河南中医药大学 第一临床医学院,河南 郑州 450046
- 2. 河南中医药大学第一附属医院 耳鼻咽喉科,河南 郑州 450000
- 折叠
摘要
老年性聋是由于内耳与听皮层老化导致的感音神经性听力损失.氧化应激在老年性聋的发生和发展中起着关键的作用.衰老过程中线粒体损伤与活性氧(reaetive oxygen species.ROS)的释放相互促进,导致氧化应激以及后续多种病理生理过程,如线粒体质量控制失衡、泛素-蛋白酶体系统障碍以及细胞程序性死亡等.抗氧化剂在清除ROS、调节线粒体功能和抑制细胞程序性死亡等方面发挥作用,对于老年性聋的防治展现出巨大潜能.总结近年来氧化应激及后续细胞过程在老年性聋中的发病机制以及抗氧化剂延缓老年性聋相关的研究进展,旨在为老年性聋的治疗提供理论基础.
Abstract
Presbycusis is a sensorineural hearing loss caused by senescence of the inner ear and auditory cortex.Oxidative stress plays a key role in the occurrence and development of presbycusis.During aging,mitochondrial damage and the release of reactive oxygen species(ROS)promote each other,leading to oxidative stress and a variety of subsequent pathophysiological processes such as an imbalance in mitochondrial quality control,ubiquitin-proteasome system disorders,and programmed cell death.Antioxidants play a role in scavenging ROS,regulating mitochondrial function and inhibiting programmed cell death,and have shown great potential in the prevention and treatment of presbycusis.This review focuses on the progress of research of oxidative stress and subsequent cellu-lar processes in the pathogenesis of presbycusis and antioxidants in delaying presbycusis in order to provide a theoretical basis for its treatment.
关键词
老年性聋/氧化应激/线粒体质量控制/细胞程序性死亡Key words
Presbycusis/Oxidative stress/Mitochondrial quality control/Programmed cell death引用本文复制引用
基金项目
国家自然科学基金(81403439)
河南省科技攻关计划(222102310604)
河南省中医药科学研究专项重点课题(20-21ZY1045)
河南省高等学校重点科研项目(23A360028)
出版年
2024
NETL
NSTL
维普
万方数据