Electrical stimulation enhances mitochondrial trafficking as a neuroprotective mechanism against chemotherapy-induced peripheral neuropathy
Electrical stimulation enhances mitochondrial trafficking as a neuroprotective mechanism against chemotherapy-induced peripheral neuropathy
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DOI：
10.1016/j.isci.2024.109052
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发表时间：
2024-02-14
期刊：
影响因子：
5.8
通讯作者：
Yang，In Hong
中科院分区：
文献类型：
--
作者：
Albin，Bayne;Adhikari，Prashant;Yang，In Hong
电刺激（ESTIM）已被证明是治疗周围神经损伤相关疼痛的有效对症治疗方法。然而，ESTIM对周围神经病变的神经保护机制尚不清楚。在这项研究中，我们发现ESTIM具有增强线粒体运输的能力，作为对抗化疗诱导的周围神经病变（cipn）的神经保护机制。CIPN是抗癌化疗导致周围神经退行性变的令人虚弱和痛苦的后遗症。分析了体外化疗药物紫杉醇和奥沙利铂对两种不同抗肿瘤机制的轴突内线粒体动力学反应。线粒体运输对化疗药物治疗的反应随着远端轴突的退化而减少。使用低频ESTIM，我们观察到增强的线粒体运输是针对CIPN的神经保护机制。本研究证实ESTIM通过增加线粒体运输促进周围神经再生。
Electrical stimulation (ESTIM) has shown to be an effective symptomatic treatment to treat pain associated with peripheral nerve damage. However, the neuroprotective mechanism of ESTIM on peripheral neuropathies is still unknown. In this study, we identified that ESTIM has the ability to enhance mitochondrial trafficking as a neuroprotective mechanism against chemotherapy-induced peripheral neuropathies (CIPNs). CIPN is a debilitating and painful sequalae of anti-cancer chemotherapy treatment which results in degeneration of peripheral nerves. Mitochondrial dynamics were analyzed within axons in response to two different antineoplastic mechanisms by chemotherapy drug treatments paclitaxel and oxaliplatinin vitro. Mitochondrial trafficking response to chemotherapy drug treatment was observed to decrease in conjunction with degeneration of distal axons. Using low-frequency ESTIM, we observed enhanced mitochondrial trafficking to be a neuroprotective mechanism against CIPN. This study confirms ESTIM enhances regeneration of peripheral nerves by increased mitochondrial trafficking.