Cytokine and Growth Factor Activation In Vivo and In Vitro after Spinal Cord Injury.
Cytokine and Growth Factor Activation In Vivo and In Vitro after Spinal Cord Injury.
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DOI：
10.1155/2016/9476020
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发表时间：
2016
影响因子：
4.6
通讯作者：
Ibarra A
中科院分区：
文献类型：
--
作者：
Garcia E;Aguilar-Cevallos J;Silva-Garcia R;Ibarra A
脊髓损伤导致一系列破坏生活的有害相互关联机制，这些机制包含原发性损伤和继发性损伤。这些事件是由在炎症、转录和信号蛋白中起作用的基因上调所介导的。特别是，细胞因子和生长因子是在脊髓损伤的病理生理学中具有重要作用的信号蛋白。这些分子的促炎和抗炎作用之间的平衡在损伤的进展和结果中起着关键作用。脊髓损伤后观察到的过度炎症性Th1和Th17表型使天平向促炎环境倾斜，这加剧了损伤后存在的有害机制。这些机制包括脊髓血屏障的破坏、水肿和离子失衡，特别是细胞内钙和钠浓度、谷氨酸兴奋性毒性、自由基，以及导致以神经组织脱髓鞘和细胞凋亡为特征的神经退行性过程的炎症反应。
Spinal cord injury results in a life-disrupting series of deleterious interconnected mechanisms encompassed by the primary and secondary injury. These events are mediated by the upregulation of genes with roles in inflammation, transcription, and signaling proteins. In particular, cytokines and growth factors are signaling proteins that have important roles in the pathophysiology of SCI. The balance between the proinflammatory and anti-inflammatory effects of these molecules plays a critical role in the progression and outcome of the lesion. The excessive inflammatory Th1 and Th17 phenotypes observed after SCI tilt the scale towards a proinflammatory environment, which exacerbates the deleterious mechanisms present after the injury. These mechanisms include the disruption of the spinal cord blood barrier, edema and ion imbalance, in particular intracellular calcium and sodium concentrations, glutamate excitotoxicity, free radicals, and the inflammatory response contributing to the neurodegenerative process which is characterized by demyelination and apoptosis of neuronal tissue.
影响因子：
6.1
作者：
Fitzgerald M
通讯作者：
Fitzgerald M