The role of mitochondria in age-related hearing loss

Chen, Hengchao; Tang, Jianguo

doi:10.1007/s10522-013-9475-y

Cited by 46 publications

(32 citation statements)

References 50 publications

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“…The incidence and frequency of mtDNA point mutations and deletions increase exponentially with age and contribute to cellular senescence in humans, monkeys, and rodents, thus providing a causative link between mtDNA mutations and aging phenotypes in mammals [71]. In the cochlea, it has been hypothesized that the cochlear mitochondrial redox imbalance and mitochondrial DNA mutation and deletion might be collaboratively involved in ARHL [72]. One specific mitochondrial common deletion (mtDNA4977) is frequently observed in the temporal bone of patients with ARHL, and its measured levels are strongly correlated with the severity of ARHL [73].…”

Section: Mitochondrial Dna Mutations and Dysfunctionmentioning

confidence: 99%

Presbycusis: An Update on Cochlear Mechanisms and Therapies

Wang

Puel

2020

JCM

158

125

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Age-related hearing impairment (ARHI), also referred to as presbycusis, is the most common sensory impairment seen in the elderly. As our cochlea, the peripheral organ of hearing, ages, we tend to experience a decline in hearing and are at greater risk of cochlear sensory-neural cell degeneration and exacerbated age-related hearing impairments, e.g., gradual hearing loss, deterioration in speech comprehension (especially in noisy environments), difficulty in the localization sound sources, and ringing sensations in the ears. However, the aging process does not affect people uniformly; nor, in fact, does the aging process appear to be uniform even within an individual. Here, we outline recent research into chronological cochlear age in healthy people, and exacerbated hearing impairments during aging due to both extrinsic factors including noise and ototoxic medication, and intrinsic factors such as genetic predisposition, epigenetic factors, and aging. We review our current understanding of molecular pathways mediating ARHL and discuss recent discoveries in experimental hearing restoration and future prospects.

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Section: Mitochondrial Dna Mutations and Dysfunctionmentioning

confidence: 99%

Presbycusis: An Update on Cochlear Mechanisms and Therapies

Wang

Puel

2020

JCM

158

125

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“…[ 5 , 6 ]. As for Sod1 , it has been reported that as the amount of oxidative stress in the cells of the auditory organ increases, the amount of Sod1 also increases [ 7 , 8 ]. In addition, numerous reports have suggested that in these models, abnormal potassium channels resulting from mass transfer errors cause cell death [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

Choi

Lee

et al. 2020

IJMS

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Age-related hearing loss (ARHL) is the most common sensory disorder among the elderly, associated with aging and auditory hair cell death due to oxidative-stress-induced mitochondrial dysfunction. Although transgenic mice and long-term aging induction cultures have been used to study ARHL, there are currently no ARHL animal models that can be stimulated by intermittent environmental changes. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined on the basis of expression of hearing-loss-induced phenotypes and aging-related factors. The incidence of hearing loss was significantly higher in dual- and triple-exposure conditions than in intermittent hypoxic conditions, high-fat diet (HFD), or d-galactose injection alone. Continuous oxidative stress and HFD accelerated cellular aging. An increase in Ucp2, usually expressed during mitochondrial dysfunction, was observed. Expression of Cdh23, Slc26a4, Kcnq4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in the cells of the hearing organ. We found that intermittent hypoxia, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects the effects of intermittent environmental changes, will benefit future research on ARHL.

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“…Presbycusis is defined as the progressive decline of hearing ability during aging and causes symmetrical, bilateral, high-frequency sensorineural hearing impairment 3. As a multifactorial disorder, presbycusis is associated with a combination of environmental factors, medical history, and nuclear and mitochondrial genome variation 4–6. Presbycusis has a great impact on the quality of life of patients as it impairs communication skills and independent daily activity and, therefore, gradually diminishes psychosocial functioning 7.…”

Section: Introductionmentioning

confidence: 99%

“…Mitochondria are considered one of the main factors in the progression of presbycusis;4 these organelles are responsible for vital cellular functions, including energy production, apoptosis, cell signaling, and calcium storage. Variants in the mtDNA control region are associated with different disorders, including cancer, Huntington disease, and β-thalassemia 10–12.…”

Section: Introductionmentioning

confidence: 99%

Association of genetic variations in the mitochondrial DNA control region with presbycusis

Falah¹,

Farhadi²,

Kamrava³

et al. 2017

CIA

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BackgroundThe prominent role of mitochondria in the generation of reactive oxygen species, cell death, and energy production contributes to the importance of this organelle in the intracellular mechanism underlying the progression of the common sensory disorder of the elderly, presbycusis. Reduced mitochondrial DNA (mtDNA) gene expression and coding region variation have frequently been reported as being associated with the development of presbycusis. The mtDNA control region regulates gene expression and replication of the genome of this organelle. To comprehensively understand of the role of mitochondria in the progression of presbycusis, we compared variations in the mtDNA control region between subjects with presbycusis and controls.MethodsA total of 58 presbycusis patients and 220 control subjects were enrolled in the study after examination by the otolaryngologist and audiology tests. Variations in the mtDNA control region were investigated by polymerase chain reaction and Sanger sequencing.ResultsA total of 113 sequence variants were observed in mtDNA, and variants were detected in 100% of patients, with 84% located in hypervariable regions. The frequencies of the variants, 16,223 C>T, 16,311 T>C, 16,249 T>C, and 15,954 A>C, were significantly different between presbycusis and control subjects.ConclusionThe statistically significant difference in the frequencies of four nucleotide variants in the mtDNA control region of presbycusis patients and controls is in agreement with previous experimental evidence and supports the role of mitochondria in the intracellular mechanism underlying presbycusis development. Moreover, these variants have potential as diagnostic markers for individuals at a high risk of developing presbycusis. The data also suggest the possible presence of changes in the mtDNA control region in presbycusis, which could alter regulatory factor binding sites and influence mtDNA gene expression and copy number.

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The role of mitochondria in age-related hearing loss

Cited by 46 publications

References 50 publications

Presbycusis: An Update on Cochlear Mechanisms and Therapies

Presbycusis: An Update on Cochlear Mechanisms and Therapies

Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

Association of genetic variations in the mitochondrial DNA control region with presbycusis

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