Vascular endothelial growth factor A (VEGF-A) and related ligands (VEGF)

Vascular endothelial growth factor A (VEGF-A) is a critical signaling protein that serves as a primary regulator of angiogenesis, the process of forming new blood vessels from pre-existing ones (UniProt P15692). It belongs to a larger family of related ligands, including VEGF-B, VEGF-C, VEGF-D, and Placental Growth Factor (PGF), which collectively coordinate the development of the vascular and lymphatic systems (StatPearls, NBK430714). These ligands exert their biological effects by binding to specific cell-surface receptor tyrosine kinases, primarily VEGFR-1, VEGFR-2, and VEGFR-3, on endothelial cells (PubMed, PMID: 23673481). In healthy tissues, VEGF signaling is essential for embryonic development and wound healing; however, its dysregulation is a hallmark of various diseases. In oncology, tumors overexpress VEGF to stimulate neovascularization, ensuring a nutrient supply for growth and facilitating metastasis (PubMed, PMID: 12359445). In ophthalmology, excessive VEGF activity leads to pathological vessel growth and leakage in conditions like wet age-related macular degeneration and diabetic retinopathy (PubMed, PMID: 24737802). Therapeutic interventions, such as monoclonal antibodies (e.g., bevacizumab) and decoy receptors (e.g., aflibercept), target these ligands to sequester them and block the activation of their respective receptors, effectively inhibiting abnormal angiogenesis (FDA, Avastin Label).

Other names

Vascular permeability factorVPFVEGFVEGF-AVEGF-BVEGF-CVEGF-DPlacental growth factorPGFVEGF family

Neutralization of circulating VEGF ligands to prevent binding and activation of VEGF receptors (VEGFR-1, VEGFR-2, and VEGFR-3), thereby inhibiting downstream signaling pathways such as MAPK and PI3K/Akt that drive endothelial cell proliferation and migration (StatPearls, NBK430714).