Noise-Induced Hearing Loss

Hyun Joon Shim

doi:10.7599/hmr.2015.35.2.84

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Shim: Noise-Induced Hearing Loss

Review Article

Hanyang Medical Reviews 2015; 35(2): 84-91.

Published online: 21 May 2015

DOI: https://doi.org/10.7599/hmr.2015.35.2.84

Noise-Induced Hearing Loss

Hyun Joon Shim

Department of Otolaryngology, Eulji Medical Center, Eulji University School of Medicine, Seoul, Korea.

Correspondence to: Hyun Joon Shim. Department of Otolaryngology, Eulji Medical Center, Eulji University School of Medicine, 68 Hangeulbiseok-ro, Nowon-gu, Seoul 139-711, Korea. Tel: +82-2-970-8276, Fax: +82-2-970-8275, eardoc11@naver.com

Received 25 February 2015 Revised 6 March 2015 Accepted 13 March 2015

(open-access):

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Noise-induced hearing loss (NIHL) is the second most common cause of permanent hearing impairment after age-related hearing loss. NIHL is influenced by environmental and genetic factors and the effects of noise can be exacerbated by the administration of ototoxic drugs or exposure to chemicals. The pathophysiology of NIHL is classified as either mechanical injury or metabolic (or biochemical) injury. Exposure of cochleae to intense sounds has been found to disrupt the stereocilia on the hair cells by separating the tip links and to depolymerize actin filaments, resulting in a disturbance in signal transduction. Major mechanisms of metabolic injuries include accumulation of reactive oxygen species enhanced by oxidative stress, cochlear ischemia followed by reperfusion injury, and excitotoxicity to auditory neuron induced by excessive release of the cochlear afferent neurotransmitter, glutamate. Many studies involving therapeutic or preventive trial with antioxidants, JNK inhibitors, and NMDA antagonists have shown partial effectiveness. However, protection from noise before cochlear injury occurs is very important because damaged hair cells and auditory neurons in the mammalian cochleae are unable to regenerate.

Keywords: Hearing Loss, Noise-Induced, Cochlea, Hair Cells, Auditory, Oxidative Stress, Apoptosis

Figures and Tables

Fig. 1

Stress-activated MAPK signaling modules. The JNK and p38 MAPK are activated by dual phosphorylation on Thr and Tyr caused by members of the MAPKK group of protein kinases. The MAPKK are activated, in turn, by phosphorylation mediated by a group of MAPKKK. Stress-activated MAPK signaling modules can be created through the sequential actions of a MAPKKK, a MAPKK, and a MAPK. Ref. 30 with permission from Cell Press.

Fig. 2

Role of the JNK signaling pathway in stress-induced apoptosis. The caspase apoptotic machinery is illustrated in a simplified cartoon. Effector caspases, including caspase-3, are activated by initiator caspases that are activated by cell surface death receptors (caspase-8) and by the mitochondrial pathway (caspase-9). JNK is not required for death receptor signaling, but is required for caspase-9 activation by the mitochondrial pathway. Potential targets of JNK include members of the Bcl2 group of apoptotic regulatory proteins. Ref. 30 with permission from Cell Press.

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ORCID iDs: Hyun Joon Shim
https://orcid.org/http://orcid.org/0000-0001-9719-6959
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