Vascular endothelial growth factor A (VEGF-A) (VEGF-A)

Vascular endothelial growth factor A (VEGF-A) is a key signaling protein that acts as the primary orchestrator of angiogenesis, the process of forming new blood vessels from pre-existing ones [4, 6]. It belongs to the platelet-derived growth factor (PDGF) family and functions by binding to its high-affinity tyrosine kinase receptors, VEGFR-1 and VEGFR-2, primarily on endothelial cells [6, 12]. This binding triggers multiple intracellular pathways, including the MAPK and PI3K/Akt cascades, which promote endothelial cell proliferation, migration, survival, and increased vascular permeability [6, 16]. While essential for physiological processes like embryonic development and wound healing, VEGF-A is frequently hijacked in pathological states [4, 11]. In oncology, tumors overexpress VEGF-A to induce neovascularization, providing the necessary nutrients and oxygen for growth and facilitating metastatic spread [1, 3]. In ophthalmology, excessive VEGF-A levels drive the development of abnormal, leaky blood vessels in conditions such as neovascular age-related macular degeneration (AMD) and diabetic retinopathy, leading to vision loss [6, 13]. Therapeutic strategies targeting VEGF-A include monoclonal antibodies like bevacizumab and ranibizumab, as well as decoy receptors like aflibercept, which neutralize the ligand to block its signaling [3, 6]. While highly effective, these therapies are associated with systemic side effects such as hypertension, proteinuria, and impaired wound healing, reflecting the protein's role in maintaining normal vascular homeostasis [1, 16].

Other names

VEGFVascular permeability factorVPFFollicular cell-derived antimitogenVEGF-A-mediated angiogenesis

Neutralization of the VEGF-A ligand to prevent its binding and activation of VEGFR-1 and VEGFR-2 receptors, thereby inhibiting downstream pro-angiogenic signaling.