Lymphangiogenesis refers to the process of forming new lymphatic vessels from pre-existing ones and involves the expansion of the lymphatic system, which functions in maintaining tissue fluid balance, immune responses, and lipid transport. The lymphatic system comprises a network of specialized vessels, lymph nodes, and other lymphoid organs that transport lymph, a clear fluid containing immune cells, proteins, and waste products. Lymphatic vessels collect excess tissue fluid, filter it through lymph nodes, and ultimately return it to the bloodstream. Lymphangiogenesis is necessary for maintaining fluid homeostasis and facilitates immune surveillance by allowing immune cells to travel to lymph nodes where they encounter pathogens and initiate immune responses. Lymphangiogenesis is particularly important during embryonic development, wound healing, and tissue repair. It occurs in response to various stimuli, including inflammation, tissue injury, and the presence of growth factors such as Vascular Endothelial Growth Factor-C (VEGF-C) and VEGF-D. These growth factors bind to VEGF receptors on lymphatic endothelial cells, activating signalling pathways that promote vessel growth, migration, and branching. The receptors for VEGF-C and VEGF-D on lymphatic endothelial cells are VEGFR-2 (also known as KDR/Flk-1) and VEGFR-3 (FLT-4). Lymphatic endothelial cells proliferate and migrate toward the source of these growth factors, forming new lymphatic vessels. The expression of VEGF-C and VEGF-D is induced by various stimuli, including inflammation, tissue injury, and hypoxia. Pathological conditions can also drive lymphangiogenesis. In cancer, for example, tumour cells can release VEGF-C and VEGF-D, inducing lymphatic vessels to sprout towards the tumour. This process facilitates the entry of tumour cells into the lymphatic system, enabling them to spread to distant lymph nodes and potentially metastasize to other organs. Lymphedema is another condition in which lymphangiogenesis can be significant. Lymphedema occurs when the lymphatic system is impaired, leading to the accumulation of fluid and swelling in tissues. In response to chronic lymphatic insufficiency, lymphangiogenesis is triggered to compensate for the impaired drainage. However, this can sometimes be inadequate, leading to persistent swelling and tissue changes. Aside from VEGF-C and -D, several key molecular factors govern lymphangiogenesis. The transcription factor Prox1 is critical for determining the lymphatic endothelial cell fate during embryonic development, controls the expression of lymphatic-specific genes, and maintains lymphatic endothelial cell identity. Neuropilin-2 (NRP-2) is a co-receptor for VEGFR-3 and plays a role in lymphatic vessel guidance and branching. It enhances VEGF-C signalling and is involved in lymphatic endothelial cell migration. Transcription factors SOX18 and GATA2 are also essential for maintaining the lymphatic identity of endothelial cells and promoting lymphatic vessel development. They also regulate the expression of lymphatic-specific genes and contribute to proper lymphatic endothelial cell function. Finally, semaphorins are a failiy of secreted proteins that elsewhere play a role in axon guidance and cell migration. In the vasculature, semaphorin 3F (Sema3F) is expressed by lymphatic endothelial cells and inhibits lymphangiogenesis by repelling lymphatic endothelial cells through its receptor Neuropilin-2. We provide a wide product catalogue of research tools for investigating lymphangiogenesis, including Angiopoietin 2 antibodies, and Angiopoietin 2 ELISA Kits. Explore our full lymphangiogenesis product range below and discover more, for less.