JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY) ›› 2014, Vol. 28 ›› Issue (4): 95-99.doi: 10.6040/j.issn.1673-3770.0.2013.308

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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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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

CLC Number: 

  • R764.43
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