ARF6 and Rab11 as intrinsic regulators of axon regeneration.
ARF6 and Rab11 as intrinsic regulators of axon regeneration.
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DOI：
10.1080/21541248.2018.1457914
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发表时间：
2020-11
期刊：
影响因子：
--
通讯作者：
Eva R
中科院分区：
文献类型：
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作者：
Nieuwenhuis B;Eva R
成人中枢神经系统（CNS）轴突损伤后不能再生，因为外部抑制因素，轴突生长的内在能力低。发育中的CNS神经元具有更好的再生能力，但随着成熟而失去这种能力。这篇简短的综述总结了最近的发现，这些发现表明再生失败的一个原因是CNS神经元成熟时生长机制远离轴突的选择性分布。这些研究证明了小GTP酶ARF6和Rab11作为极化运输和轴突再生的内在调节剂的作用。ARF6激活阻止成熟CNS轴突中Rab11内体中整合素的轴突转运。减少ARF6激活允许轴突运输，并增加再生能力。这一发现为促进中枢神经系统损伤后轴突再生提供了新的靶点。
Adult central nervous system (CNS) axons do not regenerate after injury because of extrinsic inhibitory factors, and a low intrinsic capacity for axon growth. Developing CNS neurons have a better regenerative ability, but lose this with maturity. This mini-review summarises recent findings which suggest one reason for regenerative failure is the selective distribution of growth machinery away from axons as CNS neurons mature. These studies demonstrate roles for the small GTPases ARF6 and Rab11 as intrinsic regulators of polarised transport and axon regeneration. ARF6 activation prevents the axonal transport of integrins in Rab11 endosomes in mature CNS axons. Decreasing ARF6 activation permits axonal transport, and increases regenerative ability. The findings suggest new targets for promoting axon regeneration after CNS injury.