Molecular mechanisms of traumatic brain injury in children (Retracted article. See vol. 26, pg Nil_0078, 2009)
Molecular mechanisms of traumatic brain injury in children (Retracted article. See vol. 26, pg Nil_0078, 2009)
复制标题
DOI：
10.3171/foc.2008.25.10.e6
复制
发表时间：
2008-10-01
影响因子：
4.1
通讯作者：
Jagannathan, Jay
中科院分区：
文献类型：
--
作者：
Jagannathan, Pavan;Jagannathan, Jay
尽管在分子生物学和遗传学方面取得了进展，但儿童创伤性脑损伤（TBI）的确切病理生理学尚不清楚。在本文中，作者回顾了目前已知的儿童TBI的细胞内和细胞外反应，并将这些因素与未来的调查。虽然充血和血管充血一直被认为是小儿TBI的标志，但在细胞水平上，钙内流以及局部神经递质的调节似乎在其发病中起主要作用。最近的遗传和蛋白质组学研究已经确定了特定的神经营养因子以及凋亡和抗凋亡基因，这些基因似乎控制炎症和神经元损伤的进展。寻找治疗靶点最终需要彻底了解这些因素及其在蛋白质组学，基因组学和神经水平上的相互作用。
Despite advances in molecular biology and genetics, the precise pathophysiology of traumatic brain injury (TBI) in children is unknown. In this paper the authors review what is currently known about intra- and extracellular responses to pediatric TBI and relate these factors to future investigations. Although hyperemia and vascular congestion have long been thought to be the hallmarks of pediatric TBI, on a cellular level, calcium influx as well as modulation of local neurotransmitters appears to play a major role in its onset. Recent genetic and proteomic research has identified specific neurotrophic factors as well as apoptotic and antiapoptotic genes that appear to control the progression of inflammation and neuronal damage. The search for a therapeutic target will ultimately require a thorough understanding of these factors and their interplay on a proteomic, genomic, and neuromic level.