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・ Vascular dementia
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Vascular endothelial growth factor
・ Vascular endothelial growth factor (VEGF) IRES A
・ Vascular endothelial growth factor A
・ Vascular endothelial growth factor B
・ Vascular endothelial growth factor C
・ Vascular endothelial growth inhibitor
・ Vascular headache
・ Vascular Health and Risk Management
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・ Vascular myelopathy
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Vascular endothelial growth factor : ウィキペディア英語版
Vascular endothelial growth factor
Vascular endothelial growth factor (VEGF), originally known as vascular permeability factor (VPF), is a signal protein produced by cells that stimulates vasculogenesis and angiogenesis. It is part of the system that restores the oxygen supply to tissues when blood circulation is inadequate. Serum concentration of VEGF is high in bronchial asthma and diabetes mellitus.
VEGF's normal function is to create new blood vessels during embryonic development, new blood vessels after injury, muscle following exercise, and new vessels (collateral circulation) to bypass blocked vessels.
When VEGF is overexpressed, it can contribute to disease. Solid cancers cannot grow beyond a limited size without an adequate blood supply; cancers that can express VEGF are able to grow and metastasize. Overexpression of VEGF can cause vascular disease in the retina of the eye and other parts of the body. Drugs such as bevacizumab and ranibizumab can inhibit VEGF and control or slow those diseases.
VEGF is a sub-family of growth factors, to be specific, the platelet-derived growth factor family of cystine-knot growth factors. They are important signaling proteins involved in both vasculogenesis (the ''de novo'' formation of the embryonic circulatory system) and angiogenesis (the growth of blood vessels from pre-existing vasculature).
==History==
VEGF was first identified in guinea pigs, hamsters, and mice by Senger ''et al.'' in 1983.〔 It was purified and cloned by Ferrara and Henzel in 1989. VEGF alternative splicing was discovered by Tischer ''et al.'' in 1991. Between 1996 and 1997, Christinger and De Vos obtained the crystal structure of VEGF, first at 2.5 Å resolution and later at 1.9 Å.
Fms-like tyrosine kinase-1 (flt-1) was shown to be a VEGF receptor by Ferrara ''et al.'' in 1992. The kinase insert domain receptor (KDR) was shown to be a VEGF receptor by Terman ''et al.'' in 1992 as well. In 1998, neuropilin 1 and neuropilin 2 were shown to act as VEGF receptors.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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