Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss

Joint Authors

Yamasoba, Tatsuya
Fujimoto, Chisato
Kamogashira, Teru

Source

BioMed Research International

Issue

Vol. 2015, Issue 2015 (31 Dec. 2015), pp.1-7, 7 p.

Publisher

Hindawi Publishing Corporation

Publication Date

2015-03-22

Country of Publication

Egypt

No. of Pages

7

Main Subjects

Medicine

Abstract EN

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.

American Psychological Association (APA)

Kamogashira, Teru& Fujimoto, Chisato& Yamasoba, Tatsuya. 2015. Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss. BioMed Research International،Vol. 2015, no. 2015, pp.1-7.
https://search.emarefa.net/detail/BIM-1056139

Modern Language Association (MLA)

Kamogashira, Teru…[et al.]. Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss. BioMed Research International No. 2015 (2015), pp.1-7.
https://search.emarefa.net/detail/BIM-1056139

American Medical Association (AMA)

Kamogashira, Teru& Fujimoto, Chisato& Yamasoba, Tatsuya. Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss. BioMed Research International. 2015. Vol. 2015, no. 2015, pp.1-7.
https://search.emarefa.net/detail/BIM-1056139

Data Type

Journal Articles

Language

English

Notes

Includes bibliographical references

Record ID

BIM-1056139