Vascular endothelial growth factor A, placenta growth factor, and vascular endothelial growth factor B (VEGF-A, PlGF, VEGF-B)

Vascular endothelial growth factor A, placenta growth factor, and vascular endothelial growth factor B are secreted signaling proteins that belong to the VEGF family and play central roles in blood vessel formation (angiogenesis and vasculogenesis) and tissue repair. VEGF-A (often simply referred to as “VEGF”) is the principal driver of endothelial cell proliferation, migration, and vascular permeability and is essential for embryonic vascular development, with several distinct isoforms produced by alternative splicing. Placenta growth factor (PlGF), though not required for normal development, is crucial for pathological angiogenesis—recruiting progenitor and immune cells in inflammation, ischemia, and cancer, primarily through VEGFR-1. VEGF-B interacts with VEGFR-1 and is mainly involved in endothelial function and pathological vessel growth. All three act via binding to specific receptor tyrosine kinases (VEGFRs) on target cells, initiating downstream signaling cascades critical for vascular formation and remodeling. These molecules are widely targeted by anti-angiogenic drugs in cancer and other diseases, but such therapies must balance efficacy with risks of vascular side effects, impaired healing, and tissue toxicity.

Other names

VEGF-A (“VEGF” is often used as a synonym, though technically refers to the family)Placental growth factor (“PlGF”)Vascular endothelial growth factor B (“VEGF-B”)

Ligand neutralization: Antibodies, decoy receptors, or aptamers inhibiting VEGF-A, PlGF, or VEGF-B binding to receptors, blocking downstream signaling Tyrosine kinase inhibition: Small molecules inhibit VEGFR-1 and VEGFR-2 signaling