VEGFRPDGFR

VEGFRPDGFR is a term used to describe the combined consideration of two families of receptor tyrosine kinases: vascular endothelial growth factor receptors (VEGFRs) and platelet-derived growth factor receptors (PDGFRs). It is not a single molecular entity but a framework for discussing how VEGF and PDGF signaling cooperate in vascular biology and disease.

VEGFRs and PDGFRs are transmembrane RTKs. The VEGFR family includes VEGFR-1, -2, and -3, with ligands such as VEGF-A, VEGF-B, and VEGF-C/-D, among others. The PDGFR family includes PDGFR-α and -β, activated by PDGF ligands PDGF-AA, -BB, -AB, and -CC. Ligand binding promotes receptor dimerization and autophosphorylation, initiating downstream pathways such as PI3K-AKT, RAS-MAPK, and PLCγ that regulate proliferation, survival, and migration.

These receptors regulate angiogenesis, vascular permeability, pericyte recruitment, and vessel maturation. In cancer, VEGFR and PDGFR signaling support tumor blood vessel formation and stromal interactions; co-targeting can disrupt both endothelial and mural components of vessels, potentially enhancing anti-tumor effects.

Clinical relevance centers on strategies to inhibit VEGFR or PDGFR signaling. VEGFR inhibitors (including monoclonal antibodies like bevacizumab and tyrosine kinase inhibitors such as sunitinib or pazopanib) and PDGFR inhibitors (e.g., imatinib in certain contexts) are used across cancers and vascular diseases. Dual inhibition or combination approaches targeting VEGFRPDGFR axes have been explored to overcome resistance but may increase toxicity, including hypertension, thrombosis, and impaired wound healing.

In research contexts, the term is used mainly to discuss signaling crosstalk and therapeutic strategies rather than to denote a single protein. Ongoing work investigates compensatory pathways, biomarkers of response, and the balance between anti-angiogenic efficacy and normal tissue effects.