Vascular endothelial growth factor receptor

Vascular Endothelial Growth Factor Receptor (VEGFR) is a type of protein and tyrosine kinase receptor involved in the process of angiogenesis, the formation of new blood vessels from pre-existing ones. VEGFR is a key target in the treatment of diseases such as cancer and age-related macular degeneration.

Function[edit | edit source]

VEGFR is activated by the binding of Vascular Endothelial Growth Factor (VEGF), a signal protein produced by cells that stimulates the formation of blood vessels. Upon activation, VEGFR initiates a series of signal transduction pathways leading to the proliferation, migration, and survival of endothelial cells, the cells that line the interior surface of blood vessels.

Types[edit | edit source]

There are three main types of VEGFR: VEGFR-1, VEGFR-2, and VEGFR-3. Each type has a unique role in angiogenesis and lymphangiogenesis (formation of lymphatic vessels).

VEGFR-1 (also known as Flt-1) has a high affinity for VEGF but its kinase activity is relatively weak, suggesting it may function primarily as a "decoy" receptor, sequestering VEGF and preventing it from binding to VEGFR-2.
VEGFR-2 (also known as KDR or Flk-1) is the main mediator of VEGF-driven responses in endothelial cells, including cell proliferation, migration, and the formation of new blood vessels.
VEGFR-3 (also known as Flt-4) is primarily involved in lymphangiogenesis, but also plays a role in angiogenesis during early embryonic development.

Clinical Significance[edit | edit source]

Due to its role in angiogenesis, VEGFR is a major target in the treatment of diseases characterized by excessive or insufficient blood vessel formation. In cancer, for example, tumors require a blood supply to grow and spread, so inhibiting VEGFR can starve the tumor of nutrients. Similarly, in age-related macular degeneration, abnormal blood vessel growth in the eye can lead to vision loss, and VEGFR inhibitors can help prevent this.

Several VEGFR inhibitors have been approved for clinical use, including sunitinib, sorafenib, and bevacizumab. These drugs work by blocking the binding of VEGF to VEGFR, thereby inhibiting the signal transduction pathways that lead to angiogenesis.