Programmed axon degeneration: from mouse to mechanism to medicine.
Programmed axon degeneration: from mouse to mechanism to medicine.
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DOI：
10.1038/s41583-020-0269-3
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发表时间：
2020-04
期刊：
影响因子：
--
通讯作者：
Höke A
中科院分区：
文献类型：
--
作者：
Coleman MP;Höke A
沃勒变性是一种广泛存在的程序性轴突变性机制。自Wallerian变性缓慢（WldS）小鼠发现以来的三十年中，研究已经产生了关于Wallerian变性潜在的分子机制的广泛知识，证明了其参与非损伤性疾病，并发现了多种阻断其的方法。终身拯救与小鼠沃勒变性相关的致命疾病的能力;在沃勒途径中发现“可药物化”的酶，包括SARM 1和MYCBP 2（也称为PHR 1）;以及阐明蛋白质结构，以推动对潜在机制和药物开发的进一步理解。此外，新的数据表明，这些进展有可能减轻一些常见的疾病，包括化疗引起的和糖尿病周围神经病变，创伤性脑损伤和肌萎缩侧索硬化症。
Wallerian degeneration is a widespread mechanism of programmed axon degeneration. In the three decades since the discovery of the Wallerian degeneration slow (WldS) mouse, research has generated extensive knowledge of the molecular mechanisms underlying Wallerian degeneration, demonstrated its involvement in non-injury disorders and found multiple ways to block it. Recent developments have included: the detection of NMNAT2 mutations that implicate Wallerian degeneration in rare human diseases; the capacity for lifelong rescue of a lethal condition related to Wallerian degeneration in mice; the discovery of ‘druggable’ enzymes, including SARM1 and MYCBP2 (also known as PHR1), in Wallerian pathways; and the elucidation of protein structures to drive further understanding of the underlying mechanisms and drug development. Additionally, new data have indicated the potential of these advances to alleviate a number of common disorders, including chemotherapy-induced and diabetic peripheral neuropathies, traumatic brain injury, and amyotrophic lateral sclerosis.
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