Abstract

AbstractCerebral vasospasm is a deadly complication following the rupture of intracranial aneurysms. One new development in the experimental treatment of cerebral vasospasm is the looming target of signaling pathways. The pathogenesis of cerebral vasospasm involves multiple signaling pathways in proliferation, inflammation, cell death, smooth muscle phenotype changes, vascular remodeling, and contraction. A review of all of these areas is beyond the scope of this article, and as such, three systems that mediate these vascular responses have been selected: the tyrosine kinase-MAP kinase pathway, the sphingosine-1-Rho myosin light chain kinase pathway and protein kinase C.

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