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17 April 2014 12:48 pm ,
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Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
Using the two high-quality genomes that exist for Neandertals and Denisovans, researchers find clues to gene activity...
A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
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A New Suspect Behind Atherosclerosis
25 May 2005 (All day)
Researchers have found a new mechanism that may help drive atherosclerosis, the underlying cause of about half the deaths in Westernized countries. In mice, the newly discovered culprit appears to be a kind of metabolic short-circuit inside blood vessel cells. If it holds up in humans, the finding should open up a new area for atherosclerosis research and therapy.
Atherosclerosis is the primary cause of heart disease and stroke, and a common complication of diabetes and obesity. The disorder progresses as plaque—a mix of cholesterol and other substances—builds up and hardens major arteries. The risk of atherosclerosis is significantly raised by certain factors, such as smoking and high cholesterol. But for years doctors have been puzzled that many of their patients don't share these risk factors, raising questions about what's making them sick.
Endocrinologist Clay Semenkovich and his colleagues at Washington University in St. Louis, Missouri, decided to investigate the role of a cellular process called "uncoupling" in mice. Uncoupling happens in the cell's power plants, called mitochondria; proteins open up ion channels and discharge the mitochondria's energy supply, "shorting out" the mitochondria. The group wasn't sure whether these short-circuits would produce oxidative damage—which may contribute to atherosclerosis—or ease it.
Semenkovich and his team created a litter of transgenic mice prone to develop atherosclerosis; the mice also overexpressed an uncoupling protein in their blood vessels. These mice had high blood pressure, the group reports in the 25 May Nature. The researchers also found that when the mice expressing the uncoupling protein were fed a high fat "Western diet," they developed more atherosclerosis than did littermates that did not have excess uncoupling protein. The researchers now suspect that the short-circuits increase oxidative damage, which then causes an inflammatory response, leading to atherosclerosis. Semenkovich thinks the finding, if it holds up in humans, could help explain why most people with atherosclerosis have normal cholesterol levels.
"This opens up a new area of investigation that's really new and exciting," says Aldons Lusis, a geneticist at the University of California, Los Angeles. Small differences in levels of human uncoupling protein may, over a person's lifetime, gradually drive arteries to harden, he adds.