山东大学耳鼻喉眼学报 ›› 2014, Vol. 28 ›› Issue (4): 95-99.doi: 10.6040/j.issn.1673-3770.0.2013.308

• 综述 • 上一篇    下一篇

mtDNACD4977与老年性聋相关性的研究进展

刘红1, 王帅2, 王海波1   

  1. 1. 山东大学附属省立医院 耳鼻咽喉头颈外科, 山东 济南 250021;
    2. 山东大学附属省立医院 胸外科, 山东 济南 250021
  • 收稿日期:2013-11-04 出版日期:2014-08-16 发布日期:2014-08-16
  • 通讯作者: 王海波。Email：whbotologic797@163.com E-mail:whbotologic797@163.com
  • 作者简介:刘红。Email：halaye@aliyun.com
  • 基金资助:
    山东省科技发展计划（2012G0021838）；国家重点基础研究发展计划（2014CB541703）

Review on mtDNACD4977 and presbyacusis

LIU Hong1, WANG Shuai2, WANG Hai-bo1   

  1. 1. Department of Otolaryngology & Head and Neck Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China;
    2. Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China
  • Received:2013-11-04 Online:2014-08-16 Published:2014-08-16

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摘要： 半个世纪以来，老年性聋发病率在全球范围内持续增长。据美国公共卫生署统计，75岁以上的老年人约40%～66%的有听力损失，而超过80岁的老年人80%以上有听力损失[1-3]。老年性聋是随着年龄逐步进展，双耳对称性的，以感音神经性为主的慢性进行性听力减退，又称年龄相关的听力损失[4-6]。它是年龄增长后听觉器官逐步衰老的过程，是听觉系统精细结构处理信息发生障碍的过程[7]。老年性聋是由多种危险因子的长期累积损害而成，其中年龄是最重要的危险因子。而长期慢性疾病，如高血压、糖尿病能引起内耳供血的减少，也会进一步加重听力的损害[1，8-9]。随着生物医学的不断发展，许多学者发现老年性聋患者不仅伴有核基因组的改变，线粒体DNA（mitochondrial DNA，mtDNA）的突变和缺失在老年性聋的发生、发展过程中也发挥重要作用[2，6，10]。

关键词: 老年性聋, 自由基, 氧化损伤, 线粒体DNA 4977 bp

Abstract: Since half a century ago, the incidence of presbycusis grows worldwide. Based on the data from United States Public Health Service (PHS), hearing loss affects approximately 40%～66% of adults age 75 and older. Among them, more than 80% were older than 85 years old[1-3]. Presbycusis, also called age-related hearing loss, is a chronic, progressive, bilateral, symmetrical and sensorineural hearing loss[4-6]. It's a pregressive aging of auditory organs, which involves in the disorders of fine-structure in auditory system dealing with information[7]. Presbycusis is caused by long-term cumulative damage under a variety of risk factors. Age is the most important risk factor. Chronic diseases, such as diabetes and hypertension, could also cause blood supply decrease in inner ear, which further leads to the hearing damages[1,8-9]. With the development of biomedicine, many scholars have found that alternation of nuclear genome, mutation and deletion of mitochondrial DNA play significant roles in the onset and development of presbycusis[2,6,10].

Key words: Mitochondrial DNA 4977 bp, Presbyacusis, Free radical, Oxidative stress

中图分类号: 

  • R764.43
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