Targeting HMGB1/TLR4 signaling as a novel approach to treatment of cerebral ischemia.
Targeting HMGB1/TLR4 signaling as a novel approach to treatment of cerebral ischemia.
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靶向 HMGB1/TLR4 信号作为治疗脑缺血的新方法。
DOI：
10.2741/s119
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发表时间：
2010-06
期刊：
影响因子：
--
通讯作者：
杨清武
中科院分区：
文献类型：
--
作者：
杨清武
HMGB 1是一种普遍存在的高度保守的DNA结合蛋白，在维持核内稳态方面具有公认的功能。最近关于其在大脑中的信号传导功能的许多工作都集中在其促炎特性以及与已知炎症受体如Toll样受体4（TLR 4）的关系上。HMGB 1在缺血性损伤后立即大量释放到细胞外空间，随后在缺血后脑中诱导神经炎症，表明HMGB 1在脑缺血性损伤中充当新的介质。因此，许多报告指出TLR 4在缺血性脑中起关键作用。HMGB 1和TLR 4配体作为预处理刺激可能对脑缺血的预后有益。本文就HMGB 1和TLR 4在脑缺血中的作用作一综述。靶向HMGB 1/TLR 4信号通路可能为临床预防缺血性脑损伤提供新的治疗途径。
HMGB1 is a ubiquitous, highly conserved DNA-binding protein with well-established functions in the maintenance of nuclear homeostasis. Much of the recent work about its signaling functions in the brain has focused on its proinflammatory properties and relationship to known inflammatory receptors such as toll-like receptor 4 (TLR4). HMGB1 is massively released into the extracellular space immediately after ischemic insult and that it subsequently induces neuroinflammation in the postischemic brain, indicating that HMGB1 acts as a novel mediator in cerebral ischemic injury. Consistently, numerous reports point to TLR4 as a pivotal player in the ischemic brain. The use of HMGB1 and TLR4 ligand as preconditioning stimulus may be benefit of the outcome of cerebral ischemia. Therefore, this review presents the latest findings supporting the involvement of HMGB1 and TLR4 in cerebral ischemia. Targeting HMGB1/TLR4 signaling may provide a novel therapeutic approach for clinical prevention of cerebral ischemic injury.
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影响因子：
3.1
作者：
M. Lafon;F. Mégret;M. Lafage;C. Préhaud
通讯作者：
M. Lafon;F. Mégret;M. Lafage;C. Préhaud
DOI：
--
发表时间：
2007
期刊：
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
影响因子：
--
作者：
H. Rosenzweig;M. Minami;Nikola S. Lessov;S. Coste;S. L. Stevens;D. Henshall;R. Meller;R. Simon;M. Stenzel-Poore
通讯作者：
H. Rosenzweig;M. Minami;Nikola S. Lessov;S. Coste;S. L. Stevens;D. Henshall;R. Meller;R. Simon;M. Stenzel-Poore
影响因子：
120.1
作者：
C. Zuany‐Amorim;J. Hastewell;C. Walker
通讯作者：
C. Zuany‐Amorim;J. Hastewell;C. Walker
影响因子：
3.8
作者：
Agnello, D;Wang, HC;Ghezzi, P
通讯作者：
Ghezzi, P
影响因子：
4.4
作者：
Sha, Yonggang;Zmijewski, Jaroslaw;Abraham, Edward
通讯作者：
Abraham, Edward