Vascular endothelial growth factor family and placenta growth factor (VEGF family and PlGF)

The vascular endothelial growth factor family consists of several secreted glycoproteins (including VEGF-A, VEGF-B, VEGF-C, VEGF-D, and PlGF) that are the principal drivers of angiogenesis in development and disease. These ligands primarily signal through receptor tyrosine kinases—VEGFR-1 (FLT1), VEGFR-2 (KDR/FLK1), and VEGFR-3 (FLT4)—as well as co-receptors such as neuropilins. Placenta growth factor (PlGF) is a distinct member mainly binding to VEGFR-1 and is important in pathological vascularization and inflammation, especially in cancer, ischemia, and retinopathies[1][4][5][6][7]. The VEGF family and PlGF play central roles in promoting blood vessel formation, regulating endothelial function, and modulating immune cell trafficking. Excessive activity is implicated in diseases like cancer and diabetic retinopathy, while the pathway is targeted therapeutically by anti-VEGF biologics to inhibit blood vessel growth and leakage[6][4][2]. PlGF's selective interaction with VEGFR-1 distinguishes its signaling and effects from VEGF-A, and it acts as both a partner in heterodimer formation and a regulator of VEGF-A availability at VEGFRs[1][3][4]. Note: The query "VEGF family and PlGF" refers to an entire protein family and a specific ligand, not a single, standard molecular entity. For structured databases, it is preferable to use "Vascular endothelial growth factor A" (VEGF-A), "Placenta growth factor" (PlGF), or specify the particular receptor (e.g., VEGFR-1). Thus, is_incorrect is set to true because this entry merges a family and a member and lacks the canonical precision typically required for therapeutic target lists.

Other names

Vascular endothelial growth factor (VEGF)Placenta growth factor (PlGF)VEGF-AVEGF-BVEGF-CVEGF-DPGF

Ligand neutralization by monoclonal antibodies or fusion proteins, blocking interaction with VEGF receptors; Inhibition of receptor-mediated angiogenic signaling pathways