A protein called IGF-1, which is found in high levels in young people, might offer a way to prevent arteries from clogging as we age, according to early results with mice.
“The body already works to remove plaque from arteries through certain types of white blood cells called macrophages,” says Yusuke Higashi, assistant research professor at the University of Missouri School of Medicine and lead author of the study. “However, as we age, macrophages are not able to remove plaque from the arteries as easily.
“Our findings suggest that increasing IGF-1 in macrophages could be the basis for new approaches to reduce clogged arteries and promote plaque stability in aging populations.”
In previous research, Higashi and Patrice Delafontaine, dean of the School of Medicine, examined the arteries of mice fed a high-fat diet for eight weeks. IGF-1 was administered to one group of mice.
The arteries of mice with higher levels of IGF-1 had significantly less plaque than mice that did not receive the protein. Since the macrophage is a key player in the development of atherosclerosis, the researchers decided to investigate potential anti-atherosclerosis effects of IGF-1 in macrophages.
“Our current study is one of the first ever to examine a link between IGF-1 and macrophages in relation to vascular disease,” Delafontaine says. “We examined mice whose macrophages were unresponsive to IGF-1 and found that their arteries have more plaque buildup than normal mice.
“These results are consistent with the growing body of evidence that IGF-1 helps prevent plaque formation in the arteries.”
The researchers also found that the lack of IGF-1 action in macrophages changed the composition of the plaque, weakening its strength and making it more likely to rupture and cause a heart attack.
In future research, Higashi and Delafontaine plan to conduct the same study on larger animals before eventually studying human subjects. Limitations to the current study include the small animal model, and researchers say studies on larger animals genetically closer to humans will be important for furthering the development of IGF-1-based therapeutic strategies.
The study recently was published in Circulation. The National Institutes of Health and the American Heart Association funded the work.
Source: University of Missouri