Peripheral neuropathy, which is the result of nerve damage from lesions or disease, continues to be a major health concern due to the common manifestation of neuropathic pain. Most investigations into the development of peripheral neuropathy focus on key players such as voltage-gated ion channels or glutamate receptors. However, emerging evidence points to mitochondrial dysfunction as a major player in the development of peripheral neuropathy and resulting neuropathic pain. Mitochondrial dysfunction in neuropathy includes altered mitochondrial transport, mitochondrial metabolism, as well as mitochondrial dynamics. The mechanisms that lead to mitochondrial dysfunction in peripheral neuropathy are poorly understood, however, the Class IIb histone deacetylase (HDAC6), may play an important role in the process. HDAC6 is a key regulator in multiple mechanisms of mitochondrial dynamics and may contribute to mitochondrial dysregulation in peripheral neuropathy. Accumulating evidence shows that HDAC6 inhibition is strongly associated with alleviating peripheral neuropathy and neuropathic pain, as well as mitochondrial dysfunction, in in vivo and in vitro models of peripheral neuropathy. Thus, HDAC6 inhibitors are being investigated as potential therapies for multiple peripheral neuropathic disorders. Here, we review emerging studies and integrate recent advances in understanding the unique connection between peripheral neuropathy and mitochondrial dysfunction through HDAC6-mediated interactions.

中文翻译：

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HDAC6：线粒体与周围神经病变发展之间的关键联系。

周围神经病变是病变或疾病造成的神经损伤的结果，由于神经性疼痛的常见表现，它仍然是一个主要的健康问题。大多数对周围神经病变发展的研究都集中在关键因素上，例如电压门控离子通道或谷氨酸受体。然而，新的证据表明线粒体功能障碍是周围神经病变和由此产生的神经性疼痛的发生的主要因素。神经病中的线粒体功能障碍包括线粒体运输、线粒体代谢以及线粒体动力学的改变。导致周围神经病线粒体功能障碍的机制尚不清楚，然而，IIb 类组蛋白脱乙酰酶 (HDAC6) 可能在此过程中发挥重要作用。HDAC6 是线粒体动力学多种机制的关键调节因子，可能导致周围神经病中的线粒体失调。越来越多的证据表明，在周围神经病变的体内和体外模型中，HDAC6 抑制与减轻周围神经病变和神经性疼痛以及线粒体功能障碍密切相关。因此，HDAC6 抑制剂正在被研究作为多种周围神经病的潜在疗法。在这里，我们回顾了新兴研究，并整合了最新进展，通过 HDAC6 介导的相互作用来理解周围神经病变和线粒体功能障碍之间的独特联系。