11/14/2023 0 Comments Vegfr2 wet amd genetic linkPhysiological angiogenesis is an essential feature of embryogenesis, wound healing and tissue regeneration. One class of receptor–ligand interaction occurs on the endothelium, a specialised cell type that lines all blood vessels in metazoan species from man to fish. Both processes are highly dependent on regulation by vascular endothelial growth factors (VEGFs) and their interaction with membrane receptors expressed on different cell types. Vasculogenesis is the de novo formation of a vascular network whereas angiogenesis is sprouting of new blood vessels from pre-existing ones. This review provides a rational basis towards reconciling VEGF and VEGFR structure and function in developing new therapeutics for a diverse range of ailments. As targeting VEGF-VEGFR activation holds much therapeutic promise, we examine the structural basis for anti-angiogenic therapy using small-molecule compounds such as tyrosine kinase inhibitors that block VEGFR activation and downstream signalling. Here, we use a structural viewpoint to summarise our current knowledge of VEGF-VEGFR activation and signal transduction. VEGF-A binds with high affinity to two VEGF receptor tyrosine kinases (VEGFR1, VEGFR2) and with lower affinity to co-receptors called neuropilin-1 and neuropilin-2 (NRP1, NRP2). As angiogenesis can be subverted in many disease states, including tumour development and progression, there is much interest in understanding the mechanistic basis for how VEGF-A regulates cell and tissue function. The VEGF-A family member promotes vasculogenesis and angiogenesis, processes which are essential for vascular development and physiology. Vascular endothelial growth factors (VEGFs) bind to membrane receptors on a wide variety of cells to regulate diverse biological responses.
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