Why do cholesterol and fat build up inside arteries instead of flowing out of the body as waste? Scientists at the Oklahoma Medical Research Foundation are studying how the immune system plays a role in that buildup and if there’s a way to alter the process.
Macrophages are cells in the immune system that usually act as “good guys,” said OMRF researcher Mike Kinter, Ph.D. They absorb viruses and bacteria and bits of broken cells to move them safely out of the bloodstream. But when they take in low-density lipoprotein (LDL, often known as “bad cholesterol”), the macrophages become part of the problem.
“Rather than taking LDL out of the body, macrophages eat it up and turn themselves into foam cells,” he said. “Foam cells then attach to the insides of blood vessels and begin piling up. Unfortunately, that pileup creates a plaque that causes the arteries to become blocked and changes how they work.”
The disease is called atherosclerosis, and it’s a common condition of aging, he said. The real problem lies less in the buildup of plaques—though that can be an issue—and more in what happens when chunks of the plaque break off, forming the blood clots that cause heart attacks and strokes.
In a new paper in the journal PLoS One, Kinter found that macrophages are “too good” at their jobs and that by surviving their encounter with LDL, these “good guys” become an active part of the disease.
“Plaque buildup creates a vicious cycle, so we’re interested in breaking that cycle,” he said. “As we continue our research, we’re looking for ways to intervene in the formation of foam cells that would allow macrophages to absorb the LDL and then gracefully leave the system without contributing to atherosclerosis.”
If the research is successful, it could lead to medications that prevent hardening of arteries and reduce the risk of deadly blood clots.
Research assistant Caroline Kinter is lead author on the paper and Fleming Scholars Halee Patel and Jillian Lundie contributed to the research. The research was funded by grant No. R01AG016339 from the National Institute on Aging, a part of the National Institutes of Health.
