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氨基糖苷类耳毒性的细胞机制

Cellular mechanisms of aminoglycoside ototoxicity.

作者信息

Warchol Mark E

机构信息

Department of Otolaryngology, Washington University School of Medicine, St Louis, Missouri 63110, USA.

出版信息

Curr Opin Otolaryngol Head Neck Surg. 2010 Oct;18(5):454-8. doi: 10.1097/MOO.0b013e32833e05ec.

Abstract

PURPOSE OF REVIEW

To summarize advances in the study of the interaction between sensory hair cells and aminoglycoside antibiotics.

RECENT FINDINGS

Aminoglycosides enter hair cells through mechanotransduction channels and initiate an active signaling pathway that leads to cell death. Early expression of heat shock proteins can protect hair cells from aminoglycosides, although signaling from surrounding supporting cells appears to promote hair cell death. Studies of certain human deafness mutations have revealed new insights into the role of mitochondria in aminoglycoside ototoxicity.

SUMMARY

The cellular mechanisms of aminoglycoside ototoxicity continue to be an active topic of research and newly developed animal models offer great promise for future advances. Nevertheless, proven clinical methods for the prevention of ototoxic injury are not yet available.

摘要

综述目的

总结感觉毛细胞与氨基糖苷类抗生素相互作用研究的进展。

最新发现

氨基糖苷类通过机械转导通道进入毛细胞,并启动导致细胞死亡的活跃信号通路。热休克蛋白的早期表达可保护毛细胞免受氨基糖苷类的损伤,尽管周围支持细胞发出的信号似乎会促进毛细胞死亡。对某些人类耳聋突变的研究揭示了线粒体在氨基糖苷类耳毒性中作用的新见解。

总结

氨基糖苷类耳毒性的细胞机制仍然是一个活跃的研究课题,新开发的动物模型为未来的进展带来了很大希望。然而,尚未有经过验证的预防耳毒性损伤的临床方法。

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