Endothelial angiogenesis

Endothelial angiogenesis is the physiological process of forming new blood vessels from pre-existing ones, primarily mediated by the activation, proliferation, and migration of endothelial cells [1, 6]. This process is essential for normal development and tissue repair but becomes pathologically activated in diseases such as cancer, where it facilitates tumor growth and metastasis through the 'angiogenic switch,' and in neovascular eye diseases like wet age-related macular degeneration [1, 11]. The primary molecular pathway governing this process is the Vascular Endothelial Growth Factor (VEGF) and its receptors (VEGFRs), which serve as the main targets for pharmacological intervention [6, 11]. Anti-angiogenic drugs, including monoclonal antibodies like bevacizumab and small-molecule tyrosine kinase inhibitors like sunitinib, aim to disrupt this signaling to starve tumors of nutrients or prevent abnormal vessel growth in the retina [11, 12]. Despite their clinical efficacy, these agents are associated with significant safety concerns, including hypertension, bleeding, and impaired wound healing, due to the inhibition of the VEGF pathway's role in maintaining normal vascular homeostasis [4, 9]. Note: Endothelial angiogenesis is a biological process rather than a single molecular target.

Other names

AngiogenesisNeovascularizationSprouting angiogenesisBlood vessel formationVascular endothelial growth factor signaling pathway

Inhibition of the VEGF/VEGFR signaling pathway to suppress the formation of new blood vessels [11].