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Review Article

Genetic and ethnic modulation of cardiovascular toxicity of vascular endothelial growth factor inhibitors

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Pages 46-56 | Received 07 Jul 2017, Accepted 13 Sep 2017, Published online: 27 Sep 2017

Figures & data

Table 1. Vascular endothelial growth factor inhibitors.

Figure 1. Vascular endothelial growth factor (VEGF) and its associated signal pathways maintain vascular homeostasis through promoting endothelial cell proliferation, inducing two vasodilators, nitric oxide and prostacyclin, and reducing endothelin-1, a vasoconstrictor.

Figure 1. Vascular endothelial growth factor (VEGF) and its associated signal pathways maintain vascular homeostasis through promoting endothelial cell proliferation, inducing two vasodilators, nitric oxide and prostacyclin, and reducing endothelin-1, a vasoconstrictor.

Figure 2. By blocking vascular endothelial growth factors (VEGFs), their receptors, or signal pathways, VEGF inhibitors undermine endothelial cell integrity and the balance between vasodilation and vasoconstriction, leading to hypertension, cardiac ischemia, thromboembolism, heart failure and microangiopathy.

Figure 2. By blocking vascular endothelial growth factors (VEGFs), their receptors, or signal pathways, VEGF inhibitors undermine endothelial cell integrity and the balance between vasodilation and vasoconstriction, leading to hypertension, cardiac ischemia, thromboembolism, heart failure and microangiopathy.

Table 2. Potential effects of genetic polymorphism on hypertension induced by vascular endothelial growth factor inhibitors.

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