TY - GEN
T1 - Mitogen-activated protein kinases in cerebral vasospasm after subarachnoid hemorrhage
T2 - A review
AU - Suzuki, Hidenori
AU - Hasegawa, Yu
AU - Kanamaru, Kenji
AU - Zhang, John H.
N1 - Funding Information:
This study was partially supported by grants (NS053407) from the National Institutes of Health to J.H.Z.
PY - 2011
Y1 - 2011
N2 - 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. Emphasis Type=«Italic»>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.
AB - 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. Emphasis Type=«Italic»>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.
KW - Cerebral vasospasm
KW - Mitogen-activated protein kinase
KW - Signaling transduction
KW - Subarachnoid hemorrhage
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U2 - 10.1007/978-3-7091-0353-1_23
DO - 10.1007/978-3-7091-0353-1_23
M3 - Conference contribution
C2 - 21116928
SN - 9783709103524
T3 - Acta Neurochirurgica, Supplementum
SP - 133
EP - 139
BT - Early Brain Injury or Cerebral Vasospasm
PB - Springer-Verlag Wien
ER -