Vascular endothelial growth factor (VEGF) is a hypoxia-inducible protein that plays a crucial role in angiogenesis and vascular permeability. In human glioblastomas, VEGF is highly expressed in perinecrotic palisading cells, and its gene expression is significantly enhanced under hypoxic conditions. Hypoxia is believed to be the primary driver of VEGF gene expression in glioblastoma cells, leading to tumor angiogenesis and edema formation. The disruption of the VEGF/VEGF receptor signal transduction pathway is a potential therapeutic approach to inhibit tumor angiogenesis and edema in glioblastoma patients. VEGF is a specific mitogen for endothelial cells and has been shown to induce angiogenesis both in vitro and in vivo. It is also a potent vascular permeability factor, contributing to the peritumoral edema observed in malignant gliomas. VEGF exerts its effects through two high-affinity tyrosine kinase receptors, VEGFR-1 and VEGFR-2, which are essential for its biological functions.Vascular endothelial growth factor (VEGF) is a hypoxia-inducible protein that plays a crucial role in angiogenesis and vascular permeability. In human glioblastomas, VEGF is highly expressed in perinecrotic palisading cells, and its gene expression is significantly enhanced under hypoxic conditions. Hypoxia is believed to be the primary driver of VEGF gene expression in glioblastoma cells, leading to tumor angiogenesis and edema formation. The disruption of the VEGF/VEGF receptor signal transduction pathway is a potential therapeutic approach to inhibit tumor angiogenesis and edema in glioblastoma patients. VEGF is a specific mitogen for endothelial cells and has been shown to induce angiogenesis both in vitro and in vivo. It is also a potent vascular permeability factor, contributing to the peritumoral edema observed in malignant gliomas. VEGF exerts its effects through two high-affinity tyrosine kinase receptors, VEGFR-1 and VEGFR-2, which are essential for its biological functions.