Mitogen-Activated Protein Kinases in Cerebral Vasospasm After Subarachnoid Hemorrhage: A Review

被引:31
|
作者
Suzuki, Hidenori [1 ]
Hasegawa, Yu [1 ]
Kanamaru, Kenji [2 ]
Zhang, John H. [1 ,3 ]
机构
[1] Loma Linda Univ, Sch Med, Dept Physiol, Risley Hall,Room 223, Loma Linda, CA 92354 USA
[2] Suzuka Kaisei Hosp, Dept Neurosurg, Suzuka, Japan
[3] Loma Linda Univ, Sch Med, Dept Neurosurg, Loma Linda, CA 92354 USA
基金
美国国家卫生研究院;
关键词
Cerebral vasospasm; Mitogen-activated protein kinase; Signaling transduction; Subarachnoid hemorrhage; VASCULAR SMOOTH-MUSCLE; RABBIT BASILAR ARTERY; HEAT-SHOCK PROTEINS; SIGNAL-TRANSDUCTION; UP-REGULATION; CEREBROSPINAL-FLUID; INDUCED CONTRACTION; MODEL; PHOSPHORYLATION; PATHWAYS;
D O I
10.1007/978-3-7091-0353-1_23
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Mitogen-activated protein kinases (MAPKs) have been implicated in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage. The goal of this review is to bring together recent diverse data concerning the roles of MAPKs in cerebral vasospasm and to consider the future research. Method: A review of publications in the National Library of Medicine and National Institutes of Health database was conducted in August 2009 using specific keyword search terms pertaining to subarachnoid hemorrhage and MAPKs. Findings: There are nine in vitro studies and 17 in vivo studies published. Most of previous studies used MAPK inhibitors or their upstream molecule inhibitors, and showed that MAPK inhibitions prevented vasospasm. The MAPK cascade appears to interact with other signaling molecules, and MAPK may be an important final common pathway for the signaling transduction during cerebral vasospasm. However, the mechanism by which MAPK causes sustained vascular smooth muscle contraction remains unclear. In addition, the role of endogenous MAPK inhibitors, MAPK phosphatases, has not been investigated in cerebral vasospasm. Conclusions: The experimental data support the causative role of MAPK in cerebral vasospasm and warrant further research.
引用
收藏
页码:133 / +
页数:4
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