atherosclerosis

Researchers at the University of Missouri have found a potential key to preventing fat and cholesterol build-up in the wall of arteries contributing to heart disease.

The study, recently published in the journal Circulation, has identified Insulin-Like Growth Factor-1 – also known as IGF-1 – as a novel therapy target against the clogging of arteries in aging populations.

Their preliminary findings show that increasing levels of this protein in patients presenting atherosclerosis could reduce the amount of plaque in their arteries through certain types of white blood cells called macrophages.

The body works to remove plaque by sending the macrophages as immune mediators to clean up cholesterol deposits in arteries. But as we age, macrophages aren’t able to get rid of plaque as efficiently as they used to.

The research team tested specifically whether IGF-1, which is naturally found in high levels among adolescents, could assist macrophages in removing plaque from arteries.

In a previous study at at the MU School of Medicine, the lead author of the study Yusuku Higashi conducted an eight weeks experiment on mice fed a high-fat diet and whose macrophages were IGF-1 optimised.

Higashi found that the arteries of animals who received high levels of IGF-1 had significantly less plaque than the control group.

Not only did the research scientists observed that IGF-1 reduces plaque formation, they also noted that it could change the composition of the plaque. A lack of IGF-1 appears to weaken its strength and making it more likely to rupture and cause a heart attack.

The results could, however, be also attributed to a more beneficial apolipoprotein ratio through the absence of carbohydrates in the diet, as the latest lipidology research indicates that atherosclerosis is a lipoprotein-mediated disease modifiable with the diet.

Further research envisioned by Higashi and his colleagues involves examining the link between IGF-1 and macrophages in larger animals genetically closer to humans, in order to encourage the development of IGF-1-based therapeutic interventions for the treatment of atherosclerosis and cardiovascular disease.