山东大学耳鼻喉眼学报 ›› 2024, Vol. 38 ›› Issue (1): 72-78.doi: 10.6040/j.issn.1673-3770.0.2022.518

• 综述 • 上一篇    下一篇

氧化应激在老年性聋发病机制中的研究进展

周颖东1,张梦娴1,王青玲1,康浩然2,郭向东2   

  1. 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
  • 发布日期:2024-01-12
  • 通讯作者: 郭向东. E-mail: guoxiangdong0618@126.com

Progress of research of oxidative stress in the pathogenesis of presbycusis

ZHOU Yingdong1, ZHANG Mengxian1, WANG Qingling1, KANG Haoran2, GUO Xiangdong2   

  1. 1. School of the 1st Clinical Medical Sciences, Henan University of Chinese Medicine, Zhengzhou 450046, Henan, China2. Department of Otorhinolaryngology, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, Henan, China
  • Published:2024-01-12

PDF (PC)

157

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。

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

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 cellular processes in the pathogenesis of presbycusis and antioxidants in delaying presbycusis in order to provide a theoretical basis for its treatment.

Key words: Presbycusis, Oxidative stress, Mitochondrial quality control, Programmed cell death

中图分类号: 

  • R764.35
[1] 郭向东, 王青玲, 张梦娴, 等. 基于自噬与凋亡平衡探讨补肾活血汤对衰老耳蜗毛细胞株HEI-OC1的保护作用[J]. 中国老年学杂志, 2022, 42(2): 371-376. doi:10.3969/j.issn.1005-9202.2022.02.031 GUO Xiangdong, WANG Qingling, ZHANG Mengxian, et al. Protective effect of Bushen Huoxue Decoction on aging cochlear hair cell line HEI-OC1 based on autophagy and apoptosis balance[J]. Chinese Journal of Gerontology, 2022, 42(2): 371-376. doi:10.3969/j.issn.1005-9202.2022.02.031
[2] Qi F, Zhang RS, Chen J, et al. Down-regulation of Cav1.3 in auditory pathway promotes age-related hearing loss by enhancing calcium-mediated oxidative stress in male mice[J]. Aging, 2019, 11(16): 6490-6502. doi:10.18632/aging.102203
[3] Han BA, Zhou T, Tu YQ, et al. Correlation between mitochondrial DNA 4977 bp deletion and presbycusis: a system review and meta-analysis[J]. Medicine, 2019, 98(27): e16302. doi:10.1097/MD.0000000000016302
[4] Du ZD, He L, Tu CM, et al. Mitochondrial DNA 3, 860-bp deletion increases with aging in the auditory nervous system of C57BL/6J mice[J]. ORL J Otorhinolaryngol Relat Spec, 2019, 81(2/3): 92-100. doi:10.1159/000499475
[5] Kim MJ, Haroon S, Chen GD, et al. Increased burden of mitochondrial DNA deletions and point mutations in early-onset age-related hearing loss in mitochondrial mutator mice[J]. Exp Gerontol, 2019, 125: 110675. doi:10.1016/j.exger.2019.110675
[6] Zhang Y, Huang S, Dai X, et al. SOD2 alleviates hearing loss induced by noise and kanamycin in mitochondrial DNA4834-deficient rats by regulating PI3K/MAPK signaling[J]. Curr Med Sci, 2021, 41(3): 587-596. doi:10.1007/s11596-021-2376-4
[7] Li J, Dai X, He XL, et al. Effect of SOD2 methylation on mitochondrial DNA4834-bp deletion mutation in marginal cells under oxidative stress[J]. Bosn J Basic Med Sci, 2020, 20(1): 70-77. doi:10.17305/bjbms.2019.4353
[8] Miwa T, Wei FY, Tomizawa K. Cdk5 regulatory subunit-associated protein 1 knockout mice show hearing loss phenotypically similar to age-related hearing loss[J]. Mol Brain, 2021, 14(1): 82. doi:10.1186/s13041-021-00791-w
[9] 魏薇, 杨丽辉, 熊伟, 等. 老年性聋小鼠耳蜗带状突触损伤特点及机制研究[J]. 中华耳科学杂志, 2019, 17(2): 198-202. doi:10.3969/j.issn.1672-2922.2019.02.011 WEI Wei, YANG Lihui, XIONG Wei, et al. Characteristics of cochlear ribbon synapses damage in aging mice and possible mechanisms[J]. Chinese Journal of Otology, 2019, 17(2): 198-202. doi:10.3969/j.issn.1672-2922.2019.02.011
[10] 索安奇,杨欣欣. 线粒体自噬与头颈部鳞状细胞癌关系的研究进展[J]. 山东大学耳鼻喉眼学报, 2023, 37(3): 111-117. doi: 10.6040/j.issn.1673-3770.0.2022.147 SUO Anqi, YANG Xinxin. Research progress on the relationship between mitochondrial autophagy and squamous cell carcinoma of the head and neck[J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2023, 37(3): 111-117. doi: 10.6040/j.issn.1673-3770.0.2022.147
[11] Jiao LL, Du XX, Li Y, et al. Role of mitophagy in neurodegenerative diseases and potential tagarts for therapy[J]. Mol Biol Rep, 2022, 49(11): 10749-10760. doi:10.1007/s11033-022-07738-x
[12] Youn CK, Jun Y, Jo ER, et al. Age-related hearing loss in C57BL/6J mice is associated with mitophagy impairment in the central auditory system[J]. Int J Mol Sci, 2020, 21(19): 7202. doi:10.3390/ijms21197202
[13] Oh J, Youn CK, Jun Y, et al. Reduced mitophagy in the cochlea of aged C57BL/6J mice[J]. Exp Gerontol, 2020, 137: 110946. doi:10.1016/j.exger.2020.110946
[14] Kim YJ, Choo OS, Lee JS, et al. BCL2 interacting protein 3-like/NIX-mediated mitophagy plays an important role in the process of age-related hearing loss[J]. Neuroscience, 2021, 455: 39-51. doi:10.1016/j.neuroscience.2020.12.005
[15] Cho SI, Jo ER, Song H. Urolithin A attenuates auditory cell senescence by activating mitophagy[J]. Sci Rep, 2022, 12(1): 7704. doi:10.1038/s41598-022-11894-2
[16] Lin HQ, Xiong H, Su ZW, et al. Inhibition of DRP-1-dependent mitophagy promotes cochlea hair cell senescence and exacerbates age-related hearing loss[J]. Front Cell Neurosci, 2019, 13: 550. doi:10.3389/fncel.2019.00550
[17] Xiong H, Chen SJ, Lai L, et al. Modulation of miR-34a/SIRT1 signaling protects cochlear hair cells against oxidative stress and delays age-related hearing loss through coordinated regulation of mitophagy and mitochondrial biogenesis[J]. Neurobiol Aging, 2019, 79: 30-42. doi:10.1016/j.neurobiolaging.2019.03.013
[18] 张依, 王文俊, 杨安怀. SIRT1激动剂白藜芦醇在眼部疾病中的研究进展[J]. 山东大学耳鼻喉眼学报, 2022, 36(2): 151-156. doi: 10.6040/j.issn.1673-3770.0.2021.070 ZHANG Yi, WANG Wenjun, YANG Anhuai. Research progress of SIRT1 activation by resveratrol in ocular diseases[J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2022, 36(2): 151-156. doi: 10.6040/j.issn.1673-3770.0.2021.070
[19] Pang JQ, Xiong H, Ou YK, et al. SIRT1 protects cochlear hair cell and delays age-related hearing loss via autophagy[J]. Neurobiol Aging, 2019, 80: 127-137. doi:10.1016/j.neurobiolaging.2019.04.003
[20] Li Q, Zang YZ, Sun ZW, et al. Long noncoding RNA Gm44593 attenuates oxidative stress from age-related hearing loss by regulating miR-29b/WNK1[J]. Bioengineered, 2022, 13(1): 573-582. doi:10.1080/21655979.2021.2012062
[21] Hao SJ, Wang L, Zhao K, et al. Rs1894720 polymorphism in MIAT increased susceptibility to age-related hearing loss by modulating the activation of miR-29b/SIRT1/PGC-1α signaling[J]. J Cell Biochem, 2019, 120(4): 4975-4986. doi:10.1002/jcb.27773
[22] Xie W, Shu T, Peng HS, et al. LncRNA H19 inhibits oxidative stress injury of cochlear hair cells by regulating miR-653-5p/SIRT1 axis[J]. Acta Biochim Biophys Sin(Shanghai), 2022, 54(3): 332-339. doi:10.3724/abbs.2022018
[23] Su ZW, Xiong H, Pang JQ, et al. LncRNA AW112010 promotes mitochondrial biogenesis and hair cell survival: implications for age-related hearing loss[J]. Oxid Med Cell Longev, 2019: 6150148. doi:10.1155/2019/6150148
[24] Kim HJ, Cao W, Oh GS, et al. Augmentation of cellular NAD+ by NQO1 enzymatic action improves age-related hearing impairment[J]. Aging Cell, 2019, 18(5): e13016. doi:10.1111/acel.13016
[25] Wu H, Sun HY, He ZH, et al. The effect and mechanism of 19S proteasome PSMD11/Rpn6 subunit in D-Galactose induced mimetic aging models[J]. Exp Cell Res, 2020, 394(1): 112093. doi:10.1016/j.yexcr.2020.112093
[26] Zhang Y, Huang X, Zhao XY, et al. Role of the ubiquitin C-terminal hydrolase L1-modulated ubiquitin proteasome system in auditory cortex senescence[J]. ORL J Otorhinolaryngol Relat Spec, 2017, 79(3): 153-163. doi:10.1159/000468944
[27] Villalpando-Rodriguez GE, Gibson SB. Reactive oxygen species(ROS)regulates different types of cell death by acting as a rheostat[J]. Oxid Med Cell Longev, 2021: 9912436. doi:10.1155/2021/9912436
[28] Murthy AMV, Robinson N, Kumar S. Crosstalk between cGAS-STING signaling and cell death[J]. Cell Death Differ, 2020, 27(11): 2989-3003. doi:10.1038/s41418-020-00624-8
[29] Chen C, Zhang JY, Guo ZB, et al. Effect of oxidative stress on AIF-mediated apoptosis and bovine muscle tenderness during postmortem aging[J]. J Food Sci, 2020, 85(1): 77-85. doi:10.1111/1750-3841.14969
[30] Wang L, Liu Y, Zhang X, et al. Endoplasmic reticulum stress and the unfolded protein response in cerebral ischemia/reperfusion injury[J]. Front Cell Neurosci, 2022, 16: 864426. doi:10.3389/fncel.2022.864426
[31] Lee YY, Gil ES, Jeong IH, et al. Heat shock factor 1 prevents age-related hearing loss by decreasing endoplasmic reticulum stress[J]. Cells, 2021, 10(9): 2454. doi:10.3390/cells10092454
[32] Xu A, Shang WJ, Wang Y, et al. ALA protects against ERS-mediated apoptosis in a cochlear cell model with low citrate synthase expression[J]. Arch Biochem Biophys, 2020, 688: 108402. doi:10.1016/j.abb.2020.108402
[33] Cai H, Han BA, Hu YJ, et al. Metformin attenuates the Dgalactoseinduced aging process via the UPR through the AMPK/ERK1/2 signaling pathways[J]. Int J Mol Med, 2020, 45(3): 715-730. doi:10.3892/ijmm.2020.4453
[34] Li HC, Lu MS, Zhang HW, et al. Downregulation of REST in the cochlea contributes to age-related hearing loss via the p53 apoptosis pathway[J]. Cell Death Dis, 2022, 13(4): 343. doi:10.1038/s41419-022-04774-0
[35] Zhu RZ, Li BS, Gao SS, et al. Luteolin inhibits H2O2-induced cellular senescence via modulation of SIRT1 and p53[J]. Korean J Physiol Pharmacol, 2021, 25(4): 297-305. doi:10.4196/kjpp.2021.25.4.297
[36] 楚敏, 阎希芮, 龚永昌, 等. 耳聋左慈丸对H2O2损伤小鼠耳蜗基底膜miR-34a的作用及机制[J]. 中国药理学通报, 2021, 37(12): 1757-1762. doi:10.3969/j.issn.1001-1978.2021.12.021 CHU Min, YAN Xirui, GONG Yongchang, et al. Effects of Erlong Zuoci Wan on miR-34a in H2O2 damaged cochlear basilar membranes and mechanism research[J]. Chinese Pharmacological Bulletin, 2021, 37(12): 1757-1762. doi:10.3969/j.issn.1001-1978.2021.12.021
[37] 龚永昌, 李宁, 王艺蓉, 等. 耳聋左慈丸通过调节miR-34a对HEI-OC1听细胞自噬和凋亡的影响[J]. 中华中医药杂志, 2022, 37(2): 740-744 GONG Yongchang, LI Ning, WANG Yirong, et al. Effects of Erlong Zuoci Pills on autophagy and apoptosis of HEI-OC1 cells by regulating miR-34a[J]. China Journal of Traditional Chinese Medicine and Pharmacy, 2022, 37(2): 740-744
[38] He ZH, Li M, Fang QJ, et al. FOXG1 promotes aging inner ear hair cell survival through activation of the autophagy pathway[J]. Autophagy, 2021, 17(12): 4341-4362. doi:10.1080/15548627.2021.1916194
[39] Abdel Salam S, Mostafa F, Alnamshan MM, et al. Thymoquinone ameliorates age-related hearing loss in C57BL/6J mice by modulating Sirt1 activity and Bak1 expression[J]. Biomed Pharmacother, 2021, 143: 112149. doi:10.1016/j.biopha.2021.112149
[40] Zhao JJ, Li G, Zhao X, et al. Down-regulation of AMPK signaling pathway rescues hearing loss in TFB1 transgenic mice and delays age-related hearing loss[J]. Aging, 2020, 12(7): 5590-5611. doi:10.18632/aging.102977
[41] Sánchez-Rodríguez C, Cuadrado E, Riestra-Ayora J, et al. Polyphenols protect against age-associated apoptosis in female rat cochleae[J]. Biogerontology, 2018, 19(2): 159-169. doi:10.1007/s10522-018-9747-7
[42] Li J, Jia BW, Cheng Y, et al. Targeting molecular mediators of ferroptosis and oxidative stress for neurological disorders[J]. Oxid Med Cell Longev, 2022: 3999083. doi:10.1155/2022/3999083
[43] Chen X, Li D, Sun HY, et al. Relieving ferroptosis may partially reverse neurodegeneration of the auditory cortex[J]. FEBS J, 2020, 287(21): 4747-4766. doi:10.1111/febs.15266
[44] Zhang L, Hou NN, Chen B, et al. Post-translational modifications of p53 in ferroptosis: novel pharmacological targets for cancer therapy[J]. Front Pharmacol, 2022, 13: 908772. doi:10.3389/fphar.2022.908772
[45] Tian CW, Liu YF, Li ZS, et al. Mitochondria related cell death modalities and disease[J]. Front Cell Dev Biol, 2022, 10: 832356. doi:10.3389/fcell.2022.832356
[46] Zhao X, Quan J, Tan Y, et al. RIP3 mediates TCN- induced necroptosis through activating mitochondrial metabolism and ROS production in chemotherapy-resistant cancers[J]. Am J Cancer Res, 2021, 11(3): 729-745
[47] Uni R, Choi ME. Novel roles of necroptosis mediator receptor-interacting protein kinase 3 in kidney injury[J]. Nephron, 2022, 146(3): 259-263. doi:10.1159/000517732
[48] Lyu AR, Kim TH, Park SJ, et al. Mitochondrial damage and necroptosis in aging cochlea[J]. Int J Mol Sci, 2020, 21(7): 2505. doi:10.3390/ijms21072505
[49] Su ZW, Xiong H, Liu Y, et al. Transcriptomic analysis highlights cochlear inflammation associated with age-related hearing loss in C57BL/6 mice using next generation sequencing[J]. PeerJ, 2020, 8: e9737. doi:10.7717/peerj.9737
[50] Kishino A, Hayashi K, Maeda M, et al. Caspase-8 regulates endoplasmic reticulum stress-induced necroptosis independent of the apoptosis pathway in auditory cells[J]. Int J Mol Sci, 2019, 20(23): 5896. doi:10.3390/ijms20235896
[51] Choi ME, Price DR, Ryter SW, et al. Necroptosis: a crucial pathogenic mediator of human disease[J]. JCI Insight, 2019, 4(15): e128834. doi:10.1172/jci.insight.128834
[52] Yang ZY, Zhang Y, Yang SL, et al. Low-dose resveratrol inhibits RIPK3-mediated necroptosis and delays the onset of age-related hearing loss[J]. Front Pharmacol, 2022, 13: 910308. doi:10.3389/fphar.2022.910308
[1] 索安奇,杨欣欣. 线粒体自噬与头颈部鳞状细胞癌关系的研究进展[J]. 山东大学耳鼻喉眼学报, 2023, 37(3): 111-117.
[2] 李孟婷,何书喜,王华. 炎症因子在圆锥角膜中的研究进展[J]. 山东大学耳鼻喉眼学报, 2023, 37(2): 151-158.
[3] 苏杰,杨馥宇,李猛,陈荟茹,蒋利生,王丽香. GLP-1诱导的自噬对糖尿病大鼠视网膜病变的保护作用[J]. 山东大学耳鼻喉眼学报, 2022, 36(5): 30-34.
[4] 张依,王文俊，杨安怀. SIRT1激动剂白藜芦醇在眼部疾病中的研究进展[J]. 山东大学耳鼻喉眼学报, 2022, 36(2): 151-156.
[5] 付奕豪,徐逸轩,严宏,张婕. 谷氧还蛋白在眼病中的作用研究进展[J]. 山东大学耳鼻喉眼学报, 2021, 35(3): 125-130.
[6] 宋凡,黄炜峻,许华俊,关建,易红良. 阻塞性睡眠呼吸暂停综合征患者颈动脉弹性与氧化应激反应的关系[J]. 山东大学耳鼻喉眼学报, 2019, 33(4): 99-104.
[7] 张转,刘涛,白治丽,周长明. 氧化应激与噪音性聋发病机制及治疗进展[J]. 山东大学耳鼻喉眼学报, 2017, 31(5): 101-103.
[8] 李小波,曹忠胜,辛洁,谢辰,陈锐. 罗格列酮对间歇性低氧小鼠氧化应激及认知功能的作用研究[J]. 山东大学耳鼻喉眼学报, 2017, 31(1): 45-49.
[9] 李延忠. 肥胖与阻塞性睡眠呼吸暂停[J]. 山东大学耳鼻喉眼学报, 2016, 30(5): 1-4.
[10] 李兰根, 伟伟, 张玉凤, 格日乐图, 杨佳, 张艳梅. SIRT1抗视网膜色素上皮细胞氧化应激作用的实验研究[J]. 山东大学耳鼻喉眼学报, 2015, 29(6): 56-59.
[11] 刘红, 王帅, 王海波. mtDNACD4977与老年性聋相关性的研究进展[J]. 山东大学耳鼻喉眼学报, 2014, 28(4): 95-99.
[12] 毕宏生,李树杰,崔 彦,王 慧 . 茶多酚防治STZ诱导的大鼠糖尿病性白内障的机制[J]. 山东大学耳鼻喉眼学报, 2008, 22(1): 1-05 .
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
网站版权所有 © 2018 《山东大学耳鼻喉眼学报》编辑部　
地址：山东省济南市山大南路27号（250100）电话：+86-0531-88366912 E-mail: ebhxb@sdu.edu.cn
本系统由北京玛格泰克科技发展有限公司设计开发