The National Heart, Lung and Blood Institute has awarded OMRF scientist Hong Chen, Ph.D., a four-year, $1.6 million grant to further study the role of epsins in the development and progression of atherosclerosis.
Epsins are proteins involved in the creation of new blood vessels and the process that leads to deadly plaque accumulating in arteries—or atherosclerosis. Atherosclerosis of the coronary arteries, or coronary heart disease, is the top killer of both men and women in the United States.
“We found these proteins, Epn1 and Epn2, recruit macrophages to arterial damage,” said Chen, an associate member in OMRF’s Cardiovascular Biology Research Program. “Macrophages are immune cells, and when they’re summoned, they kind of get stuck and begin eating up lipids, which are fats in the bloodstream.”
Once they’ve absorbed as much fat as they can, the macrophages die. But instead of being swept out of the system, they stick to the sides of arteries and form plaque. When that plaque builds up, it causes atherosclerosis, hardening and narrowing the arteries.
Plaque can also rupture and break apart, potentially causing an aneurysm, stroke or heart attack, she said.
Chen’s lab, working with researchers at Yale and the University of San Diego La Jolla, will look for more evidence that suppressing epsins can prevent or reverse atherosclerosis.
“Ultimately, the goal is to find new treatments for atherosclerosis, and we think digging deep into the precise mechanisms of epsins will lead us to them,” she said.
Once researchers understand exactly how epsins initiate and propel the growth of plaque, Chen said they’ll be able to find treatments that target the process without causing unintended consequences.
The work will be funded by grant No. R01HL118676 from the NHLBI, a part of the National Institutes of Health.