Written by: Silke Schmidt
The diminutive size of our aortic valve — just shy of a quarter — belies its essential role in pushing oxygen-rich blood from the heart into the aorta, our body’s largest vessel, and from there to all other organs. Yet for decades, researchers have focused less on damaged valves than on atherosclerosis, the gradual hardening of the blood vessels themselves.
Thanks, in part, to pigs at the University of Wisconsin–Madison’s Arlington Agricultural Research Station, scientists now are catching up on understanding the roots of calcific aortic valve disease (CAVD).
“For a long time, people thought CAVD was just the valvular equivalent of atherosclerosis,” says Kristyn Masters, a professor of biomedical engineering at UW–Madison. “Today, we know that valve cells are quite unique and distinct from the smooth muscle cells in our blood vessels, which explains why some treatments for atherosclerosis, such as statins, don’t work for CAVD, and why the search for drugs has to start from scratch.” Read more.
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