Endostatin may stop the progression of atherosclerosisBMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7190.1030b (Published 17 April 1999) Cite this as: BMJ 1999;318:1030
The experimental drug endostatin, which is being developed for its ability to shrink cancerous tumours by inhibiting the development of new blood vessels, is also showing promise in stopping atherosclerosis.
Researchers have found that endostatin significantly reduced atherosclerosis in genetically susceptible mice. In the 16 week experiment which involved 73 mice, the researchers tested endostatinas well as TNP-470, another substance known to inhibit the growth of capillaries, in animals fed a high cholesterol diet. Animals that had been treated with one of the two drugs had 70%to 85%less plaque deposition in their aortas than those that were untreated (Circulation 1999;99:1726-32).
The inhibitors had much less effect if they were given too early (before the plaques reached substantial size and needed new blood vessels to grow further) or too late (after the plaques were mature).
Endostatin is a naturally occurring protein that blocks the formation of blood vessels. Withouta blood supply tumours in animals stop growing and sometimes regress completely.
Atherosclerotic heart disease also involves unwanted tissue growth. “By blocking this perhaps we can alter the progression of the disease,”said Dr Moulton. In addition, cutting off the blood supply from a plaque may reduce the likelihoodthat the plaque will eventually rupture. However, she pointed out that further research will be needed to determine whether treatment with angiogenesis inhibitors in people at high risk of heart disease can affect the development of large atherosclerotic deposits.
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