Vascular endothelial growth factor A and Vascular endothelial growth factor B (VEGF-A / VEGF-B)

Vascular endothelial growth factor A (VEGF-A) and Vascular endothelial growth factor B (VEGF-B) are key members of the VEGF family of glycoproteins, which are critical regulators of blood vessel formation and maintenance [3, 16]. VEGF-A is the primary driver of angiogenesis and vasculogenesis, acting through its receptors VEGFR-1 and VEGFR-2 to promote endothelial cell proliferation, migration, and survival, while also significantly increasing vascular permeability [10, 16]. In contrast, VEGF-B primarily binds to VEGFR-1 and is recognized more for its role in cell survival, lipid metabolism, and neuroprotection rather than direct angiogenic induction [7, 17]. Pathologically, overproduction of these factors is a hallmark of tumor growth, where they facilitate the development of a blood supply to support malignancy, and in ocular diseases like age-related macular degeneration, where they cause abnormal, leaky vessel growth [2, 12]. Therapeutic strategies targeting these molecules include monoclonal antibodies and decoy receptors, such as aflibercept, which neutralize the ligands to inhibit pathological vessel formation and reduce edema [2, 19]. Clinical use of these inhibitors has revolutionized the treatment of various cancers and blinding eye diseases, though it requires careful management of systemic side effects like hypertension and proteinuria [15, 20]. Overall, the dual inhibition of VEGF-A and VEGF-B provides a potent mechanism for controlling aberrant vascularization and tissue homeostasis in diverse clinical settings [2, 12].

Other names

VEGFVPFVascular permeability factorVEGFLVRFVascular endothelial growth factor

Neutralization of circulating growth factors to prevent binding to VEGFR-1 and VEGFR-2, thereby inhibiting downstream signaling pathways such as PLCγ-PKC-MAPK and PI3K-Akt to suppress angiogenesis and vascular permeability [2, 10, 16].