FAK mediates noise-induced loss of auditory hair cell function and survival

项目摘要 长期以来，线粒体功能障碍一直被认为是噪声导致的脑功能丧失的潜在机制 听力敏感度(NIHL)然而，导致这种功能障碍的启动过程却知之甚少。 这一建议是建立在新的和重要的发现基础上的，涉及到外周血细胞线粒体动力学的变化 大声音暴露后的毛细胞。线粒体是高度动态的细胞器，不断地进行分裂 和融合来适应细胞环境的变化，而且越来越明显的是 线粒体形态直接关系到线粒体的功能，因此，线粒体的健康和存活 牢房。本文建议的研究将检验潜在的整合素信号通路，以诱导 线粒体分裂活性。具体地说，我们将研究FAK作为噪声诱导的中介的作用 过度刺激毛囊细胞导致细胞死亡和听力敏感性丧失。

Project Summary Mitochondrial dysfunction has long been recognized as an underlying mechanism of noise-induced loss of hearing sensitivity (NIHL). However, the initiating processes that lead to this dysfunction is poorly understood. This proposal is founded upon new and important findings involving changes in mitochondrial dynamics in outer hair cells after loud sound exposure. Mitochondria are highly dynamic organelles that constantly undergo fission and fusion to adapt to changes in the cellular environment, and it is becoming increasingly clear that mitochondrial morphology is directly related to mitochondrial function and, therefore, the health and survival of the cell. The studies proposed here will examine a potential integrin signaling pathway for induction of mitochondrial fission activity. Specifically, we will investigate the role of FAK as a mediator of noise-induced overstimulation of OHCs leading to cell death and loss of hearing sensitivity.