Equilibrium Research
Online ISSN : 1882-577X
Print ISSN : 0385-5716
ISSN-L : 0385-5716
菅原 一真山下 裕司
ジャーナル フリー

2005 年 64 巻 2 号 p. 50-56


It is well-known that the inner ear hair cells are easily damaged by ototoxic stresses (e.g. aminoglycosides, ischemia). Hair cell death often results in permanent hearing loss and vestibular dysfunction. To treat the inner ear diseases with loss of hair cells, we should understand the signaling pathway of sensory hair cell death and protection. In this article, I would like to discuss some recent findings about inner ear hair cell death and protection. There are many reports that hair cell death is induced in the form of apoptosis. The key molecules are caspases and c -Jun N2 terminal kinase (JNK) in the signaling pathway of hair cell death. The inhibition of these molecules can protect the hair cells against ototoxic chemicals.
The heat shock response is a fundamental mechanism of cells to cope with adverse environments, and is regulated mainly at the level of transcription by heat shock transcription factor (HSF1) in mammals. The activations of caspases and JNK are inhibited by heat shock proteins, and result in the survival of cells. Therefore, we performed experiments to analyze the role of the heat shock response in the inner ear. Our results showed that the heat shock response protected the inner era against intense noise, and that the heat shock response was regulated by HSF1. The heat shock response is the one of the potential candidates for the protection of the inner ear. But more in vivo experiments will be required for the clinical treatment of inner ear diseases.

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