LITERATURE REVIEW
Stroke is one of the major health problems worldwide and a leading cause of disability. But the treatment options for the management of stroke are limited. Thrombolytic reperfusion with recombinant tissue plasminogen activator (t-PA) is employed in acute phase in only less than 3% of all ischemic stroke patients while standard treatments involving rehabilitation provide some benefits for the recovery during chronic phase. However, many high-profile failures in a wide spectrum of pharmacologic neuroprotection trials have led to some pessimism in the field.[1] Recent findings suggest that enhancement of angiogenesis after focal cerebral ischemia may provide novel opportunities for better outcomes during stroke recovery.[2] Nowadays it is appreciated that new treatment strategies should target cerebral blood vessels and induction of angiogenesis will stimulate recovery processes including neurogenesis, synaptogenesis, and neuronal and synaptic …show more content…
Some of the major factors are vascular endothelial growth factor (VEGF), Fibroblast growth factor-2 (FGF-2/bFGF), Platelet-Derived growth factor-Beta (PDGF-beta), Transforming growth factor-beta (TGF-beta). These angiogenic peptides are found to be upregulated following ischemic insults to promote micro vessel formation and brain remodeling.[1] Among these numerous endogenous angiogenic regulators, VEGF is the prototypical and most studied proangiogenic mediator in stroke.[2, 3] VEGF is an endothelial cell-specific mitogen which also plays a role in the regulation of vascular permeability. VEGF executes its biological effect through two tyrosine kinase receptors, Flt-1 (VEGFr-1) and KDR (VEGFR-2).[15] It has been known to be the potent mediator of neurorestoration following stroke by promoting neurogenesis and
Stroke is one of the major health problems worldwide and a leading cause of disability. But the treatment options for the management of stroke are limited. Thrombolytic reperfusion with recombinant tissue plasminogen activator (t-PA) is employed in acute phase in only less than 3% of all ischemic stroke patients while standard treatments involving rehabilitation provide some benefits for the recovery during chronic phase. However, many high-profile failures in a wide spectrum of pharmacologic neuroprotection trials have led to some pessimism in the field.[1] Recent findings suggest that enhancement of angiogenesis after focal cerebral ischemia may provide novel opportunities for better outcomes during stroke recovery.[2] Nowadays it is appreciated that new treatment strategies should target cerebral blood vessels and induction of angiogenesis will stimulate recovery processes including neurogenesis, synaptogenesis, and neuronal and synaptic …show more content…
Some of the major factors are vascular endothelial growth factor (VEGF), Fibroblast growth factor-2 (FGF-2/bFGF), Platelet-Derived growth factor-Beta (PDGF-beta), Transforming growth factor-beta (TGF-beta). These angiogenic peptides are found to be upregulated following ischemic insults to promote micro vessel formation and brain remodeling.[1] Among these numerous endogenous angiogenic regulators, VEGF is the prototypical and most studied proangiogenic mediator in stroke.[2, 3] VEGF is an endothelial cell-specific mitogen which also plays a role in the regulation of vascular permeability. VEGF executes its biological effect through two tyrosine kinase receptors, Flt-1 (VEGFr-1) and KDR (VEGFR-2).[15] It has been known to be the potent mediator of neurorestoration following stroke by promoting neurogenesis and