Vascular endothelial growth factor A and Placenta growth factor (VEGF-A and PlGF)

Vascular endothelial growth factor A (VEGF-A) and Placenta growth factor (PlGF) are members of the VEGF family of growth factors, which play central roles in the regulation of angiogenesis and vascular function. VEGF-A is the principal mediator of angiogenesis, acting mainly through activation of VEGF receptor 2 (VEGFR2), but it also binds VEGFR1. PlGF is structurally related to VEGF-A but binds selectively to VEGFR1, modulating angiogenesis especially in pathological conditions such as ischemia and cancer, often by enhancing VEGF-A-driven signaling[2][3][4][5]. Both molecules are secreted proteins that can function in autocrine, paracrine, and endocrine fashions. They are primary therapeutic targets in diseases driven by pathological angiogenesis—including cancer and ocular neovascular disorders—and are targeted by multiple biologics designed to inhibit their activity[2][5]. Due to their central role in vascular biology, blockade of these factors is associated with a range of on-target toxicities affecting blood pressure, vascular integrity, and wound healing[2][5].

Other names

VEGFA and PGFVEGF (for VEGF-A before the discovery of other family members)Placental growth factorVascular permeability factor (for VEGF-A)

Neutralization of ligand (antibodies or aptamers bind VEGF-A and/or PlGF to prevent receptor activation); Ligand "trapping" with decoy receptors (e.g., aflibercept binds VEGF-A and PlGF and prevents them from activating receptors); Inhibition of receptor dimerization and downstream signaling (blocking angiogenesis and vascular permeability)