Extracellular proteolytic pathophysiology in the neurovascular unit after stroke

被引:39
|
作者
Lee, SR
Wang, XY
Tsuji, K
Lo, EH
机构
[1] Massachusetts Gen Hosp, Dept Radiol, Neuroprotect Res Lab, Boston, MA 02129 USA
[2] Massachusetts Gen Hosp, Dept Neurol, Neuroprotect Res Lab, Boston, MA 02129 USA
[3] Harvard Univ, Sch Med, Program Neurosci, Charlestown, MA 02129 USA
关键词
neuroprotection; neurovascular unit; blood-brain barrier; matrix;
D O I
10.1179/016164104X3806
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The NINDS Stroke Progress Review Group recommended a shift in emphasis from a purely neurocentric view of cell death towards a more integrative approach whereby responses in all brain cells and matrix are considered. The neurovascular unit (fundamentally comprising endothelium, astrocyte, and neuron) provides a conceptual framework where cell-cell and cell-matrix signaling underlies the overall tissue response to stroke and its treatments. Here, we briefly review recent data on extracellular proteolytic dysfunction in the neurovascular unit after a stroke. The breakdown of neurovascular matrix initiates blood-brain barrier disruption with edema and/or hemorrhage. Endothelial dysfunction amplifies inflammatory responses. Perturbation of cell-matrix homeostasis triggers multiple cell death pathways. Interactions between the major classes of extracellular proteases from the plasminogen and matrix metalloprotease families may underlie processes responsible for some of the hemorrhagic complications of thrombolytic stroke therapy. Targeting the proteolytic imbalance within the neurovascular unit may provide new approaches for improving the safety and efficacy of thrombolytic reperfusion therapy for stroke.
引用
收藏
页码:854 / 861
页数:8
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