Mechanisms of axonal injury: internodal nanocomplexes and calcium deregulation.
Mechanisms of axonal injury: internodal nanocomplexes and calcium deregulation.
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DOI：
10.1016/j.molmed.2010.02.002
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发表时间：
2010-04
影响因子：
13.6
通讯作者：
Stys PK
中科院分区：
文献类型：
--
作者：
Stirling DP;Stys PK
轴突变性导致许多神经系统疾病的发病率，包括中风、神经创伤和多发性硬化症。由于CNS神经元再生能力有限，结合轴突损伤导致临床残疾的观察，促使人们努力研究轴突变性的机制。钙离子从轴突外流入是损伤的关键介质。最近大量的池内轴突钙隔离在“轴浆网”已被报道。这些钙储存在位于髓磷脂下沿着节间的多分子“纳米复合物”的控制下。在疾病期间这些复合物的过度激活可能导致从轴突内储存的Ca的致命释放。丰富的受体药理学提供了诱人的治疗选择，针对这些纳米复合物在许多疾病中，轴突变性是突出的。
Axonal degeneration causes morbidity in many neurological conditions, including stroke, neurotrauma and multiple sclerosis. Given the limited ability of CNS neurons to regenerate, combined with the observation that axonal damage causes clinical disability, has spurred efforts to investigate the mechanisms of axonal degeneration. Ca influx from outside the axon is a key mediator of injury. More recently substantial pools of intra-axonal Ca sequestered in “axoplasmic reticulum” have been reported. These Ca stores are under control of multimolecular “nanocomplexes” located along the internode under the myelin. Overactivation of these complexes during disease may lead to lethal release of Ca from intra-axonal stores. Rich receptor pharmacology offers tantalizing therapeutic options targeting these nanocomplexes in the many diseases where axonal degeneration is prominent.
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影响因子：
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通讯作者：
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影响因子：
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