Vascular endothelial growth factor signaling pathway mediators (VEGF pathway mediators)

The Vascular Endothelial Growth Factor (VEGF) signaling pathway is a fundamental regulator of angiogenesis, vasculogenesis, and lymphangiogenesis [1, 2]. It comprises a family of ligands, including VEGF-A, VEGF-B, VEGF-C, VEGF-D, and Placental Growth Factor (PlGF), which interact with three primary receptor tyrosine kinases: VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1), and VEGFR-3 (Flt-4) [3]. Among these, the VEGF-A/VEGFR-2 axis is the most significant driver of endothelial cell proliferation, migration, and vascular permeability [2, 5]. In many cancers, tumors overexpress VEGF to stimulate the formation of a dedicated blood supply, facilitating growth and metastasis [1]. In ophthalmology, excessive VEGF activity leads to neovascularization and fluid leakage in conditions like wet age-related macular degeneration [4]. Therapeutic strategies targeting this pathway include monoclonal antibodies that neutralize ligands, decoy receptors (traps), and small-molecule tyrosine kinase inhibitors (TKIs) that block downstream signaling [1, 4].

Other names

VEGF/VEGFR systemVEGF signaling componentsAngiogenic factorsVascular permeability factor signaling

Inhibition of VEGF ligands through neutralizing antibodies or decoy receptors, blockade of VEGF receptors, and inhibition of intracellular tyrosine kinase activity [1, 4].