Diffuse Axonal Injury and Oxidative Stress: A Comprehensive Review.
Diffuse Axonal Injury and Oxidative Stress: A Comprehensive Review.
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DOI：
10.3390/ijms18122600
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发表时间：
2017-12-02
影响因子：
5.6
通讯作者：
Fineschi V
中科院分区：
文献类型：
--
作者：
Frati A;Cerretani D;Fiaschi AI;Frati P;Gatto V;La Russa R;Pesce A;Pinchi E;Santurro A;Fraschetti F;Fineschi V
创伤性脑损伤（TBI）是世界上年轻人发病和死亡的主要原因之一。TBI对脑实质施加强大的旋转和平移力，这导致创伤性弥漫性轴索损伤（DAI），其负责脑肿胀和神经元死亡。TBI后，轴突变性已被确定为一个渐进的过程，其开始于轴突运输中断引起轴突肿胀，随后是继发性轴突断开和沃勒变性。轴突细胞骨架的这些改变中断了轴浆的运输机制，导致运输产物的逐渐聚集，从而产生轴突分泌和神经元稳态的改变。氧化应激导致内源性抗氧化防御机制受损在导致神经元死亡的继发性事件中起着重要作用。研究支持轴突钙稳态改变作为轴突继发性损伤的一种机制，并表明钙通道阻滞剂可以减轻继发性损伤以及继发性损伤中隐含的其他机制，并可作为治疗方法的候选者。活性氧（reactive oxygen species，ROS）介导的轴突变性主要由细胞外Ca 2+引起。通过使用外源性抗氧化剂增加防御机制可能具有神经保护作用，特别是如果它们在神经保护时间窗内给予。DAI的一个有前途的潜在治疗靶点是直接解决与脊髓损伤相关的损伤或调节充满活力的轴突能量衰竭。
Traumatic brain injury (TBI) is one of the world’s leading causes of morbidity and mortality among young individuals. TBI applies powerful rotational and translational forces to the brain parenchyma, which results in a traumatic diffuse axonal injury (DAI) responsible for brain swelling and neuronal death. Following TBI, axonal degeneration has been identified as a progressive process that starts with disrupted axonal transport causing axonal swelling, followed by secondary axonal disconnection and Wallerian degeneration. These modifications in the axonal cytoskeleton interrupt the axoplasmic transport mechanisms, causing the gradual gathering of transport products so as to generate axonal swellings and modifications in neuronal homeostasis. Oxidative stress with consequent impairment of endogenous antioxidant defense mechanisms plays a significant role in the secondary events leading to neuronal death. Studies support the role of an altered axonal calcium homeostasis as a mechanism in the secondary damage of axon, and suggest that calcium channel blocker can alleviate the secondary damage, as well as other mechanisms implied in the secondary injury, and could be targeted as a candidate for therapeutic approaches. Reactive oxygen species (ROS)-mediated axonal degeneration is mainly caused by extracellular Ca2+. Increases in the defense mechanisms through the use of exogenous antioxidants may be neuroprotective, particularly if they are given within the neuroprotective time window. A promising potential therapeutic target for DAI is to directly address mitochondria-related injury or to modulate energetic axonal energy failure.
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影响因子：
4.8
作者：
Anderson, RE;Hansson, LO;Settergren, G
通讯作者：
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DOI：
10.1016/j.jmr.2011.09.022
发表时间：
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期刊：
JOURNAL OF MAGNETIC RESONANCE SERIES B
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DOI：
10.1097/00005072-199906000-00003
发表时间：
1999-06-01
影响因子：
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DOI：
10.1097/nen.0b013e3181da84db
发表时间：
2010-05-01
影响因子：
3.2
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