VEGFtekijän

VEGFtekijän, also known as vascular endothelial growth factor (VEGF), is a protein that plays a crucial role in the growth and development of blood vessels. It is a key mediator in angiogenesis, the process by which new blood vessels form from existing ones. VEGF is produced by various cell types, including endothelial cells, macrophages, and tumor cells, and it acts on endothelial cells to stimulate their proliferation, migration, and differentiation into new blood vessels.

VEGF is a member of the VEGF family, which includes several related proteins such as VEGF-A, VEGF-B, VEGF-C, VEGF-D, and placental growth factor (PlGF). Each of these proteins has distinct biological functions and tissue distributions. VEGF-A is the most studied and is known to be a potent angiogenic factor, while PlGF is primarily involved in placental development.

VEGF signaling is mediated through specific receptors, known as VEGFRs (VEGF receptors). There are three main VEGFRs: VEGFR-1 (also known as Flt-1), VEGFR-2 (also known as KDR/Flk-1), and VEGFR-3. VEGFR-2 is the primary receptor for VEGF-A and is essential for angiogenesis. VEGFR-3 is primarily activated by VEGF-C and VEGF-D and is involved in lymphangiogenesis, the formation of lymphatic vessels.

VEGF and its receptors are involved in various physiological and pathological processes. In normal physiology, VEGF plays a role in wound healing, fertility, and embryonic development. In pathological conditions, VEGF is implicated in diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, VEGF is often overexpressed, leading to the formation of new blood vessels that supply the tumor with nutrients and oxygen, promoting tumor growth and metastasis.

VEGF is also a target for therapeutic interventions. Anti-VEGF agents, such as bevacizumab (Avastin) and ranibizumab (Lucentis), have been developed to inhibit VEGF signaling and are used to treat various diseases, including cancer, diabetic retinopathy, and age-related macular degeneration. These agents work by binding to VEGF and preventing it from interacting with its receptors, thereby inhibiting angiogenesis.