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Cellular mechanisms of aminoglycoside ototoxicity.

机译:氨基糖苷耳毒性的细胞机制。

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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.
机译:审查的目的:总结感官毛细胞和氨基糖苷类抗生素之间相互作用的研究进展。最近的发现:氨基糖苷类通过机械转导通道进入毛细胞,并启动了导致细胞死亡的活跃信号通路。尽管周围的支持细胞发出的信号似乎促进了毛细胞的死亡,但热激蛋白的早期表达可以保护毛细胞免受氨基糖苷类的影响。对某些人类耳聋突变的研究揭示了线粒体在氨基糖苷耳毒性中的作用的新见解。概述:氨基糖苷耳毒性的细胞机制仍然是研究的一个活跃主题,新开发的动物模型为未来的发展提供了广阔的前景。然而,尚无用于预防耳毒性损伤的行之有效的临床方法。

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