Insulin-associated neuroinflammatory pathways as therapeutic targets for traumatic brain injury.
Insulin-associated neuroinflammatory pathways as therapeutic targets for traumatic brain injury.
复制标题
DOI：
10.1016/j.mehy.2013.11.028
复制
发表时间：
2014-02
影响因子：
4.7
通讯作者：
Borlongan, Cesar V.
中科院分区：
文献类型：
--
作者：
Cerecedo-Lopez, Christian D.;Kim-Lee, Jennifer H.;Hernandez, Diana;Acosta, Sandra A.;Borlongan, Cesar V.
创伤性脑损伤（TBI）的特征是对头部的突然打击或力量交换，可分为轻度，中度和重度。TBI后的继发性细胞死亡表现为缺血样模式，包括神经炎症。清道夫受体分化簇（CD）36是能够转导细胞内信号以促进不同细胞类型内的炎症机制的脂质相关蛋白。CD36的表达和活化与糖尿病继发性血脂异常密切相关。糖尿病（DM）已被证明是TBI的共病因素，因为有糖尿病史的患者比非糖尿病患者表现出更严重的脑损伤和更慢的TBI恢复。事实上，通过使用胰岛素严格调节血清葡萄糖促进了TBI患者的更好结果。基于这些最新的发现，我们现在提出的假设，CD36通过糖尿病胰岛素相关的途径是密切参与TBI慢性病理。
Traumatic brain injury (TBI) is characterized by an abrupt blow or exchange of force against the head and can be categorized as mild, moderate, and severe. The secondary cell death after TBI displays ischemic-like patterns including neuroinflammation. The scavenger receptor cluster of differentiation (CD) 36 is a lipid-associated protein capable of transducing intracellular signals to promote inflammatory mechanisms within different cell types. Expression and activation of CD36 is closely related to dyslipidemia secondary to diabetes. Diabetes mellitus (DM) has been documented as a co-morbidity factor in TBI, in that patients with a history of diabetes present with more severe brain damage and slower recovery from TBI than non-diabetic patients. Indeed, a strict regulation of blood serum glucose by the use of insulin promotes a better outcome for TBI patients. Based on these recent findings, we now advance the hypothesis that CD36 via DM insulin-associated pathways is closely involved in TBI chronic pathology.
登录
查看更多内容
DOI：
10.1523/jneurosci.5399-12.2013
发表时间：
2013-04-03
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Bachstetter AD;Rowe RK;Kaneko M;Goulding D;Lifshitz J;Van Eldik LJ
通讯作者：
Van Eldik LJ
CD36介导了对β-淀粉样蛋白的先天宿主反应。
影响因子：
15.3
作者：
El Khoury, JB;Moore, KJ;Means, TK;Leung, J;Terada, K;Toft, M;Freeman, MW;Luster, AD
通讯作者：
Luster, AD
影响因子：
5
作者：
Grebe, Alena;Latz, Eicke
通讯作者：
Latz, Eicke
影响因子：
6
作者：
Coraci, IS;Husemann, J;El Khoury, JB
通讯作者：
El Khoury, JB
影响因子：
4.7
作者：
Cho S;Kim E
通讯作者：
Kim E