Angiogenesis - the process by which new blood vessels form from pre-existing ones - plays critical roles in embryonic development, repair of tissue damage, and pathological conditions like cancer. Angiogenesis is regulated by a series of molecular signals, primarily driven by pro-angiogenic growth factors. The key players are the vascular endothelial growth factor (VEGF) family, which includes VEGF-A, VEGF-B, VEGF-C, and VEGF-D. VEGF-A is a potent inducer of angiogenesis, binding to its receptor, VEGFR2, on the surface of endothelial cells lining existing blood vessels. VEGF binding triggers a series of signalling events within endothelial cells that lead to endothelial cell proliferation, migration, and sprouting. Other growth factors like fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and angiopoietins play additional roles in angiogenesis. Collectively, VEGF and other growth factors initiate a series of intracellular signalling pathways, including the Ras-MAPK, PI3K-AKT and Notch pathways, to regulate endothelial cell proliferation, migration, and differentiation. The Ras-MAPK pathway is involved in cell proliferation in response to VEGF signalling, whilst the VEGF-PI3K-AKT pathway is critical for cell migration, leading to the activation of AKT, which controls cell motility and cytoskeletal rearrangements. Notch signalling plays a key role in vessel sprouting and branching by regulating endothelial cell fate decisions and guiding tip cells (leading cells of sprouts) and stalk cells (cells forming the vessel's trunk). Finally, Rho GTPases- a family of small GTP-binding proteins including RhoA, Rac1, and Cdc42 that act as molecular switches- also play important roles in various aspects of angiogenesis, contributing significantly to both the regulation of endothelial cell migration, recruitment of pericytes and their attachment to newly formed blood vessels. At the cellular level, angiogenesis involves a series of distinct steps. Angiogenesis is first triggered by an imbalance between oxygen demand and supply, leading to the secretion of pro-angiogenic factors, especially VEGF, by surrounding hypoxic cells or tissues. VEGF induces the expression of matrix metalloproteinases (MMPs) and the basement membrane surrounding existing blood vessels is remodelled to allow new vessels to sprout. Among the MMPs, MMP-2 (also known as gelatinase A) and MMP-9 (gelatinase B) have been particularly implicated in the initial stages of angiogenesis. These two MMPs specifically degrade type IV and type V collagen, the major components of the basement membrane surrounding blood vessels. Activated endothelial cells then undergo proliferation and migration toward the pro-angiogenic gradient of growth factors. Endothelial cells next form sprouts that protrude into the surrounding tissue. Endothelial cells align and elongate, eventually connecting and forming a lumen that matures into a functional vessel. Pericytes and smooth muscle cells are subsequently recruited to stabilize the newly formed vessel, promoting its integrity. Finally, other growth factors are involved in angiogenesis, aside from VEGFs. Angiopoietin-1 (Ang-1) binding to its receptor Tie-2 helps stabilize blood vessels and enhance vascular integrity, whilst Ang-2 can also regulate vessel destabilization by affecting interactions with Ang-1. Transforming growth factor-beta (TGF-β) also contributes to vessel maturation and stabilization, promoting pericyte and smooth muscle cell recruitment to vessels. We provide a wide product range of research reagents for studying angiogenesis, including CD45 antibodies, CD31 antibodies, CD34 antibodies, Osteopontin ELISA Kits, and IL8 ELISA Kits. Explore our full angiogenesis product range below and discover more, for less. Alternatively, you can explore our Endothelial Cell Markers, Growth Factors, and Adhesion & ECM product ranges.