Vascular endothelial growth factor family (VEGF family)

The **Vascular endothelial growth factor family** (VEGF family) is a group of structurally related, secreted glycoproteins that play a central role in the regulation of blood vessel and lymphatic vessel formation, vascular permeability, and tissue regeneration. The mammalian VEGF family consists of five primary members: VEGF-A, placenta growth factor (PGF), VEGF-B, VEGF-C, and VEGF-D, each with distinct and sometimes overlapping roles in angiogenesis, lymphangiogenesis, embryonic development, and disease states[1][2][3][4][5][6]. These growth factors exert their activity by binding to specific receptor tyrosine kinases (VEGFR-1, VEGFR-2, VEGFR-3) and co-receptors such as neuropilins, triggering intracellular signaling cascades that regulate endothelial cell proliferation, migration, survival, and permeability[3][4]. VEGF signaling is tightly regulated in normal physiology but is dysregulated in many pathologies, most notably contributing to tumor angiogenesis in cancer and neovascularization in eye diseases[2][3][4]. As such, the VEGF pathway is a validated and widely targeted axis for therapeutic intervention using monoclonal antibodies, receptor decoys, and kinase inhibitors, though safety concerns related to normal vascular processes remain significant[4]. Biomarker strategies frequently measure VEGF-A or isoform levels for prognosis or monitoring therapeutic response, particularly in oncology and cardiovascular medicine[1][2].

Other names

Vascular endothelial growth factorsVEGFs

Inhibition of VEGF binding to VEGF receptors (e.g., monoclonal antibodies, receptor decoys) - Inhibition of VEGF receptor tyrosine kinase activity (small molecule inhibitors) - Suppression of angiogenesis and vascular permeability