Autophagy Attenuates Noise-Induced Hearing Loss by Reducing Oxidative Stress

Hu, Yuan; Wang, Xianren; Hill, Kayla; Chen, Jun; Lemasters, John J.; Yang, Shi‐Ming; Sha, Su-Hua

doi:10.1089/ars.2014.6004

Cited by 139 publications

(161 citation statements)

References 57 publications

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“…In addition, more HC loss (mainly OHCs) was observed in mutant mice compared to controls two weeks after noise exposure. Consistent with previous reports [43–45], our results indicated that OHCs are more vulnerable to noise compared to IHCs. Failed recovery of ABR thresholds in mutant mice may be partially caused by permanent HC loss in the cochlea.…”

Section: Discussionsupporting

confidence: 93%

Loss of Myh14 Increases Susceptibility to Noise-Induced Hearing Loss in CBA/CaJ Mice

Zhang

Jin

et al. 2016

Neural Plasticity

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MYH14 is a member of the myosin family, which has been implicated in many motile processes such as ion-channel gating, organelle translocation, and the cytoskeleton rearrangement. Mutations in MYH14 lead to a DFNA4-type hearing impairment. Further evidence also shows that MYH14 is a candidate noise-induced hearing loss (NIHL) susceptible gene. However, the specific roles of MYH14 in auditory function and NIHL are not fully understood. In the present study, we used CRISPR/Cas9 technology to establish a Myh14 knockout mice line in CBA/CaJ background (now referred to as Myh14−/− mice) and clarify the role of MYH14 in the cochlea and NIHL. We found that Myh14−/− mice did not exhibit significant hearing loss until five months of age. In addition, Myh14−/− mice were more vulnerable to high intensity noise compared to control mice. More significant outer hair cell loss was observed in Myh14−/− mice than in wild type controls after acoustic trauma. Our findings suggest that Myh14 may play a beneficial role in the protection of the cochlea after acoustic overstimulation in CBA/CaJ mice.

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Section: Discussionsupporting

confidence: 93%

Loss of Myh14 Increases Susceptibility to Noise-Induced Hearing Loss in CBA/CaJ Mice

Zhang

Jin

et al. 2016

Neural Plasticity

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“…Under normal physiological conditions, 1–2% of molecular oxygen is reduced to superoxide, a free radical that can be converted to less toxic hydrogen peroxide by mitochondrial superoxide dismutase (SOD2) or proceed in a reaction chain to even more detrimental compounds such as the hydroxyl radical. Increased ROS generation in cochlear fluids and tissues, including in OHCs and the stria vascularis, by traumatic noise is well documented and other free radicals in the form of reactive nitrogen species (RNS) derived from nitric oxide (NO) are also present 15–17 . ROS may persist for 7–10 days and spread apically from the basal end of the organ of Corti, thus widening the area of damage well after an exposure has been terminated.…”

Section: Molecular Mechanisms Of Neurosensory Damagementioning

confidence: 99%

“…On the other hand, moderate noise exposure increased ROS in OHCs only marginally thus prompting autophagy, a cellular homeostatic response 17 . The autophagy marker LC3 was upregulated in OHCs of CBA/J mice, and the fact that only a TTS but no permanent damage was observed, suggested autophagy as a protective mechanism against NIHL.…”

Section: Molecular Mechanisms Of Neurosensory Damagementioning

confidence: 99%

“…The autophagy marker LC3 was upregulated in OHCs of CBA/J mice, and the fact that only a TTS but no permanent damage was observed, suggested autophagy as a protective mechanism against NIHL. However, excessive oxidative stress, as under PTS-noise conditions, overwhelmed the beneficial potential of autophagy in OHCs and led to OHC death and NIHL 17 .…”

Section: Molecular Mechanisms Of Neurosensory Damagementioning

confidence: 99%

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Emerging therapeutic interventions against noise-induced hearing loss

Sha

Schacht

2016

Expert Opinion on Investigational Drugs

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106

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Introduction Noise-induced hearing loss (NIHL) due to industrial, military, and recreational noise exposure is a major, but also potentially preventable cause of acquired hearing loss. For the United States it is estimated that 26 million people (15% of the population) between the ages of 20 and 69 have a high-frequency NIHL at a detriment to the quality of life of the affected individuals and great economic cost to society. Areas covered This review outlines the pathology and pathophysiology of hearing loss as seen in humans and animal models. Results from molecular studies are presented that have provided the basis for therapeutic strategies successfully applied to animals. Several compounds emerging from these studies (mostly antioxidants) are now being tested in field trials. Expert opinion Although no clinically applicable intervention has been approved yet, recent trials are encouraging. In order to maximize protective therapies, future work needs to apply stringent criteria for noise exposure and outcome parameters. Attention needs to be paid not only to permanent NIHL due to death of sensory cells but also to temporary effects that may show delayed consequences. Existing results combined with the search for efficacious new therapies should establish a viable treatment within a decade.

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“…SIRT1 inactivates p53 and subsequently inhibits p53-mediated apoptosis induced by ROS through deacetylation of p53 [Luo et al, 2001;Vaziri et al, 2001]. Because ROS are well known as major contributors to NIHL [Henderson et al, 2006;Yuan et al, 2015], SIRT1 should be considered a potential target for treatment of NIHL and protection of cochlear hair cells. Moreover, our previous studies demonstrated that SIRT1 is abundantly expressed in the cochlea and downregulated with aging, which is correlated with activation of cochlear p53, cochlear hair cell loss, and age-related hearing loss [Xiong et al, 2014[Xiong et al, , 2015.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Promotes Recovery of Hearing following Intense Noise Exposure by Enhancing Cochlear SIRT1 Activity

Xiong

et al. 2017

Audiol Neurotol

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The sirtuin SIRT1 is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase known to have protective effects against a wide range of neurological disorders. In the present study, we discovered that C57BL/6 mice fed a long-term diet supplemented with high-dose resveratrol exhibited increased cochlear SIRT1 activity and presented a better recovery of hearing and less loss of hair cells after intense noise exposure compared with those fed a standard chew. Moreover, resveratrol attenuated cochlear SIRT1 decrease and reduced oxidative stress in the cochlea after noise exposure. These results suggest a considerable therapeutic potential of resveratrol for the treatment of noise-induced hearing loss.

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Autophagy Attenuates Noise-Induced Hearing Loss by Reducing Oxidative Stress

Cited by 139 publications

References 57 publications

Loss of Myh14 Increases Susceptibility to Noise-Induced Hearing Loss in CBA/CaJ Mice

Loss of Myh14 Increases Susceptibility to Noise-Induced Hearing Loss in CBA/CaJ Mice

Emerging therapeutic interventions against noise-induced hearing loss

Resveratrol Promotes Recovery of Hearing following Intense Noise Exposure by Enhancing Cochlear SIRT1 Activity

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