Concepts for regulation of axon integrity by enwrapping glia.
Concepts for regulation of axon integrity by enwrapping glia.
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DOI：
10.3389/fncel.2013.00256
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发表时间：
2013-12-19
影响因子：
5.3
通讯作者：
Beirowski B
中科院分区：
文献类型：
--
作者：
Beirowski B
长轴突及其包裹的胶质细胞（EG;雪旺细胞（SC）和少突胶质细胞（OLG））形成独特的复合结构，其充当神经系统中电和化学信息的运输管道。特殊的细胞结构在一个巨大的长度，以及其大量的能量需求，使这个管道特别容易受到有害的改变。在一系列神经退行性疾病中，由于SC和OLG的异常，相对较早地观察到独立于神经元细胞体的长轴突的退行性变。这导致了最相关的疾病症状，并强调了这些神经胶质细胞对轴突完整性的关键作用，但潜在的机制仍然难以捉摸。了解轴突退化的原因和方式的探索现在是以疾病为导向的研究的一个关键前沿。如果认识到在病理情况下轴突和其侧翼神经胶质之间不可分割的联系，这一挑战最有可能导致重大进展。在这篇综述中，我汇编了最近的进展，我们了解的分子程序管理轴突变性，和EG的非细胞自主轴突完整性的影响机制。一个特别的重点是放在新兴的证据表明，EG培育长轴突凭借其密切的联系，释放的营养物质，和神经代谢耦合。这些功能缺陷的纠正具有稳定周围神经系统和中枢神经系统（PNS和CNS）中的各种神经元疾病中的轴突的潜力。
Long axons and their enwrapping glia (EG; Schwann cells (SCs) and oligodendrocytes (OLGs)) form a unique compound structure that serves as conduit for transport of electric and chemical information in the nervous system. The peculiar cytoarchitecture over an enormous length as well as its substantial energetic requirements make this conduit particularly susceptible to detrimental alterations. Degeneration of long axons independent of neuronal cell bodies is observed comparatively early in a range of neurodegenerative conditions as a consequence of abnormalities in SCs and OLGs . This leads to the most relevant disease symptoms and highlights the critical role that these glia have for axon integrity, but the underlying mechanisms remain elusive. The quest to understand why and how axons degenerate is now a crucial frontier in disease-oriented research. This challenge is most likely to lead to significant progress if the inextricable link between axons and their flanking glia in pathological situations is recognized. In this review I compile recent advances in our understanding of the molecular programs governing axon degeneration, and mechanisms of EG’s non-cell autonomous impact on axon-integrity. A particular focus is placed on emerging evidence suggesting that EG nurture long axons by virtue of their intimate association, release of trophic substances, and neurometabolic coupling. The correction of defects in these functions has the potential to stabilize axons in a variety of neuronal diseases in the peripheral nervous system and central nervous system (PNS and CNS).
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影响因子：
5.3
作者：
Babetto, Elisabetta;Beirowski, Bogdan;Coleman, Michael P.
通讯作者：
Coleman, Michael P.
影响因子：
4.8
作者：
Bakhti, Mostafa;Winter, Christine;Simons, Mikael
通讯作者：
Simons, Mikael
DOI：
10.1523/jneurosci.4065-10.2011
发表时间：
2011-01-19
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Barrientos SA;Martinez NW;Yoo S;Jara JS;Zamorano S;Hetz C;Twiss JL;Alvarez J;Court FA
通讯作者：
Court FA
影响因子：
9.2
作者：
Avery, Michelle A;Rooney, Timothy M;Pandya, Jignesh D;Wishart, Thomas M;Gillingwater, Thomas H;Geddes, James W;Sullivan, Patrick G;Freeman, Marc R
通讯作者：
Freeman, Marc R
DOI：
10.1097/nen.0b013e3181da84db
发表时间：
2010-05-01
影响因子：
3.2
作者：
Beirowski, Bogdan;Nogradi, Antal;Coleman, Michael P.
通讯作者：
Coleman, Michael P.