A growth factor, or protein, that encourages the growth of cells on the inner walls of blood vessels (endothelial cells[1]). It appears to play an important role in angiogenesis, the development and growth of new blood vessels, which has widespread effects throughout the body.
Angiogenesis was first an area of interest for cancer researchers, most notably the pioneering researcher Dr. Judah Folkman. Cancer researchers noted that certain types of tumors secrete growth factors, such as VEGF. VEGF appears to stimulate the movement of endothelial progenitor cells, adult stem cells[2] that eventually differentiate into the cells that line the inner walls of blood vessels.
Cancer researchers reasoned that blocking VEGF and thus inhibiting angiogenesis and cutting off the blood supply to a tumor might be a way to keep tumors from thriving. An anti-VEGF drug called bevacizumab (brand name Avastin) was approved by the US Food and Drug Administration in 2004 for the treatment of colorectal cancer and was subsequently approved for the treatment of lung, kidney, and brain cancer.
VEGF appears to play a key role in the development of cardiovascular disease. VEGF levels in the bloodstream are elevated in people with high blood pressure and diabetes. In people with high blood pressure, levels of VEGF are related to measures of endothelial dysfunction (an early marker of atherosclerosis, or narrowing of the arteries due to inflammation and plaque formation) and overall cardiovascular risk. Some studies suggest that high blood glucose levels tend to raise VEGF levels in the bloodstream. Studies also suggest that VEGF may promote inflammation of the blood vessels and the clumping together of blood platelets, both of which promote cardiovascular disease.
VEGF also appears to play a key role in the development of a form of diabetic eye disease called proliferative diabetic retinopathy[3]. In proliferative diabetic retinopathy, abnormally fragile new blood vessels grow on the surface of the eye’s light-sensitive retina and tend to leak and cause fibrous scar tissue. This tissue pulls on the retina and can lead to retinal detachment and loss of vision in some cases.
High blood glucose levels damage the normal cells lining the eye’s smallest blood vessels, the capillaries, leading to “capillary closure” and a depletion of oxygen due to poor circulation. This lack of oxygen (“hypoxia”) triggers an increase in levels of VEGF in the vitreous, the clear gelatin filling most of the internal eye, which in turn promotes the growth of abnormal new blood vessels, leading to proliferative diabetic retinopathy.
VEGF has been connected to several other eye diseases as well, including certain forms of macular degeneration[4], neovascular glaucoma[5], and diabetic macular edema[6]. VEGF also appears to play a role in the development of diabetic kidney disease. Scientists hope that they may someday stop or delay the progression of diabetic eye and kidney diseases using drugs that block the action of VEGF.
VEGF has potential therapeutic effects as well. Researchers hope someday to use therapeutic angiogenesis to restore blood flow to the heart in people with coronary artery disease who aren’t responding well enough to drug therapy and are unsuitable for procedures such as coronary bypass surgery and angioplasty.
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