Stroke significantly affects white matter in the brain by impairing axon function, which results in clinical deficits. Axonal mitochondria are highly dynamic and are transported via microtubules in the anterograde or retrograde direction, depending upon axonal energy demands. Recently, we reported that mitochondrial division inhibitor 1 (Mdivi-1) promotes axon function recovery by preventing mitochondrial fission only when applied during ischemia. Application of Mdivi-1 after injury failed to protect axon function. Interestingly, L-NIO, which is a NOS3 inhibitor, confers post-ischemic protection to axon function by attenuating mitochondrial fission and preserving mitochondrial motility via conserving levels of the microtubular adaptor protein Miro-2. We propose that preventing mitochondrial fission protects axon function during injury, but that restoration of mitochondrial motility is more important to promote axon function recovery after injury. Thus, Miro-2 may be a therapeutic molecular target for recovery following a stroke.

中文翻译：

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保持线粒体的结构和动力促进缺血后白色物质的恢复。

中风会通过损害轴突功能而严重影响大脑中的白质，从而导致临床缺陷。轴突线粒体是高度动态的，并且根据轴突能量需求通过微管在顺行或逆行方向上运输。最近，我们报道线粒体分裂抑制剂1（Mdivi-1）仅在局部缺血时才通过阻止线粒体裂变来促进轴突功能恢复。受伤后应用Mdivi-1无法保护轴突功能。有趣的是，作为NOS3抑制剂的L-NIO通过减弱线粒体裂变并通过保持微管衔接蛋白Miro-2的水平来保持线粒体的运动性，从而赋予了缺血后轴突保护功能。我们建议防止线粒体裂变在受伤时保护轴突功能，但线粒体运动的恢复对于促进损伤后轴突功能的恢复更为重要。因此，Miro-2可能是中风后恢复的治疗性分子靶标。