Vascular endothelial growth factor signaling axis (VEGF signaling axis)

The Vascular endothelial growth factor (VEGF) signaling axis is the primary regulator of angiogenesis, the process by which new blood vessels form from existing vasculature [1]. This axis consists of several ligands (VEGF-A, -B, -C, -D, and PlGF) and their corresponding receptor tyrosine kinases (VEGFR-1, -2, and -3), with the VEGF-A/VEGFR-2 interaction being the most critical driver of endothelial cell proliferation, migration, and survival [2][3]. Under physiological conditions, this signaling is essential for embryonic development, wound repair, and the female reproductive cycle [4]. However, in pathological states such as cancer, tumors overexpress VEGF to induce 'angiogenic switching,' creating a chaotic vascular network that supports tumor expansion and provides a route for metastasis [5]. Therapeutic targeting of this axis, using monoclonal antibodies like bevacizumab or multi-kinase inhibitors like sunitinib, has become a standard of care in oncology and ophthalmology, though it is often associated with class-specific toxicities such as hypertension and impaired wound healing [6].

Other names

Angiogenic signaling axisVEGF/VEGFR pathwayPro-angiogenic signaling cascadeVascular endothelial growth factor pathway

Inhibition of pro-angiogenic signaling through the sequestration of circulating ligands or the competitive inhibition of intracellular receptor tyrosine kinase domains, preventing downstream activation of pathways that drive endothelial cell growth and survival.