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  Indian J Med Microbiol
 

Figure 1: The temporal effects of vascular endothelial growth factor in acute ischemic stroke. In middle cerebral artery occlusion models of acute ischemic stroke there are increases in vascular endothelial growth factor levels. In the first 4 h after acute ischemic stroke, there is vascular endothelial growth factor-mediated activation of matrix metalloproteinases causing cerebral edema and localized inflammation, thus damaging neurons and nervous system tissue. After this acute inflammatory phase, the positive effects of vascular endothelial growth factor signaling to its downstream target proteins, such as Akt, mitogen-activated protein kinase, and phosphatidyl-inositol-3-kinase, include angiogenesis and neurogenesis

Figure 1: The temporal effects of vascular endothelial growth factor in acute ischemic stroke. In middle cerebral artery occlusion models of acute ischemic stroke there are increases in vascular endothelial growth factor levels. In the first 4 h after acute ischemic stroke, there is vascular endothelial growth factor-mediated activation of matrix metalloproteinases causing cerebral edema and localized inflammation, thus damaging neurons and nervous system tissue. After this acute inflammatory phase, the positive effects of vascular endothelial growth factor signaling to its downstream target proteins, such as Akt, mitogen-activated protein kinase, and phosphatidyl-inositol-3-kinase, include angiogenesis and neurogenesis