Angiogenesis-related endothelial receptors and complexes

Angiogenesis-related endothelial receptors and complexes refer to a heterogeneous group of cell surface proteins and signaling assemblies on endothelial cells that mediate the formation of new blood vessels. The primary components include the Vascular Endothelial Growth Factor Receptor (VEGFR) family, particularly VEGFR-2, which is the major mediator of endothelial cell mitogenesis and permeability (Ferrara, 2004, Nature Medicine). Other essential receptors include the Tie family (Tie-1 and Tie-2/TEK), which regulate vascular maturation and stability through interactions with angiopoietins (UniProt, P35590). Cell adhesion molecules such as integrins (e.g., alpha-v beta-3) also play a critical role by facilitating endothelial cell adhesion and migration during vessel sprouting (Carmeliet, 2005, Nature). In pathological conditions such as cancer and neovascular eye diseases, these receptors are often overexpressed or hyper-activated, driving the growth of abnormal, leaky vessels that support tumor growth or cause vision loss (Apte et al., 2019, Cell). Therapeutic strategies targeting these complexes include monoclonal antibodies like Bevacizumab, which sequesters ligands, and small-molecule tyrosine kinase inhibitors like Sunitinib, which block intracellular signaling (PubChem, CID 5329102). While effective, these therapies are often associated with systemic side effects such as hypertension and impaired wound healing due to the inhibition of physiological vascular maintenance (Jayson et al., 2016, Lancet). Resistance to these therapies can occur through the upregulation of alternative angiogenic pathways, necessitating the development of multi-target inhibitors or combination therapies.

Other names

Angiogenic receptorsEndothelial cell surface receptorsPro-angiogenic signaling complexesVascular endothelial growth factor receptors and associated proteins

Inhibition of ligand binding to endothelial receptors (e.g., VEGF-A) or inhibition of intracellular tyrosine kinase activity to block downstream pro-angiogenic signaling pathways such as MAPK/ERK and PI3K/Akt.