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Review
. 2015:2015:617207.
doi: 10.1155/2015/617207. Epub 2015 Mar 22.

Reactive oxygen species, apoptosis, and mitochondrial dysfunction in hearing loss

Teru Kamogashira  1 , Chisato Fujimoto  1 , Tatsuya Yamasoba  1
Affiliations
Review

Reactive oxygen species, apoptosis, and mitochondrial dysfunction in hearing loss

Teru Kamogashira et al. Biomed Res Int. 2015.

Abstract

Reactive oxygen species (ROS) production is involved in several apoptotic and necrotic cell death pathways in auditory tissues. These pathways are the major causes of most types of sensorineural hearing loss, including age-related hearing loss, hereditary hearing loss, ototoxic drug-induced hearing loss, and noise-induced hearing loss. ROS production can be triggered by dysfunctional mitochondrial oxidative phosphorylation and increases or decreases in ROS-related enzymes. Although apoptotic cell death pathways are mostly activated by ROS production, there are other pathways involved in hearing loss that do not depend on ROS production. Further studies of other pathways, such as endoplasmic reticulum stress and necrotic cell death, are required.

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