Vascular endothelial growth factor A, Vascular endothelial growth factor B, Placental growth factor (VEGF-A, VEGF-B, PlGF)

Vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor B (VEGF-B), and placental growth factor (PlGF) are secreted glycoproteins that function as key regulators of angiogenesis and vasculogenesis. Each is a member of the VEGF family and exerts its biological effects by binding to specific cell-surface tyrosine kinase receptors on endothelial cells, primarily VEGFR-1 (FLT1) and VEGFR-2 (KDR/Flk-1). - VEGF-A is the principal mediator of blood vessel formation and vascular permeability, acting mainly via VEGFR-2 and to a lesser extent VEGFR-1[1][4]. - VEGF-B and PlGF bind selectively and with high affinity to VEGFR-1, playing roles in pathological angiogenesis, inflammation, cardiovascular adaptation, and tissue remodeling[2][4][5]. - These proteins exist as disulfide-bonded homodimers with cystine-knot motifs, and multiple isoforms arise from alternative RNA splicing, especially for VEGF-A (e.g., VEGF-A121, VEGF-A165, etc.), each with distinct biophysical and receptor-binding properties[3]. - Collectively, the VEGF–VEGFR system is a validated therapeutic target, particularly in oncology (to inhibit tumor vascularization), ophthalmology, and certain cardiovascular conditions[4]. - Drugs targeting VEGF-A, VEGF-B, and PlGF block their receptor interactions and downstream signaling, disrupting processes crucial to neovascular growth and associated pathologies[4].

Other names

VEGFAVEGFBPGF (Placental growth factor)VEGF (sometimes used generically for VEGF-A)VPF (Vascular permeability factor, for VEGF-A)Placenta growth factor (for PlGF)Vascular endothelial growth factor-BVascular endothelial growth factor-A

Ligand neutralization (antibodies or traps bind VEGF-A, VEGF-B, or PlGF, preventing receptor activation) Inhibition of angiogenesis (blockade of VEGFR-1/VEGFR-2 signaling) Reduction of vascular permeability