TY - JOUR
T1 - Plasticity of cerebrovascular smooth muscle cells after subarachnoid hemorrhage
AU - Edvinsson, Lars
AU - Larsen, Stine Schmidt
AU - Maddahi, Aida
AU - Nielsen, Janne
PY - 2014/6
Y1 - 2014/6
N2 - Subarachnoid hemorrhage (SAH) is most often followed by a delayed phase of cerebral ischemia which is associated with high morbidity and mortality rates. The causes underlying this delayed phase are still unsettled, but are believed to include cerebral vasospasm, cortical spreading depression, inflammatory reactions, and microthrombosis. Additionally, a large body of evidence indicates that vascular plasticity plays an important role in SAH pathophysiology, and this review aims to summarize our current knowledge on the phenotypic changes of vascular smooth muscle cells of the cerebral vasculature following SAH. In light of the emerging view that the whole cerebral vasculature and the cells of the brain parenchyma should be viewed as one integrated neurovascular network, phenotypical changes are discussed both for the cerebral arteries and the microvasculature. Furthermore, the intracellular signaling involved in the vascular plasticity is discussed with a focus on the Raf-MEK1/2-ERK1/2 pathway which seems to play a crucial role in SAH pathology.
AB - Subarachnoid hemorrhage (SAH) is most often followed by a delayed phase of cerebral ischemia which is associated with high morbidity and mortality rates. The causes underlying this delayed phase are still unsettled, but are believed to include cerebral vasospasm, cortical spreading depression, inflammatory reactions, and microthrombosis. Additionally, a large body of evidence indicates that vascular plasticity plays an important role in SAH pathophysiology, and this review aims to summarize our current knowledge on the phenotypic changes of vascular smooth muscle cells of the cerebral vasculature following SAH. In light of the emerging view that the whole cerebral vasculature and the cells of the brain parenchyma should be viewed as one integrated neurovascular network, phenotypical changes are discussed both for the cerebral arteries and the microvasculature. Furthermore, the intracellular signaling involved in the vascular plasticity is discussed with a focus on the Raf-MEK1/2-ERK1/2 pathway which seems to play a crucial role in SAH pathology.
KW - Animals
KW - Cerebral Cortex
KW - Cerebrovascular Disorders
KW - Humans
KW - Muscle, Smooth, Vascular
KW - Subarachnoid Hemorrhage
U2 - 10.1007/s12975-014-0331-4
DO - 10.1007/s12975-014-0331-4
M3 - Journal article
C2 - 24449486
SN - 1868-4483
VL - 5
SP - 365
EP - 376
JO - Translational Stroke Research
JF - Translational Stroke Research
IS - 3
ER -