How eliminating a protein may help people at high risk avoid heart attacks and strokes, a new study shows.

Macrophages eat fat as Pac-Man gobbles ghosts as they go through our arteries. Fat-filled macrophages, on the other hand, can restrict blood arteries and lead to heart disease.

In a new study published in Nature Cardiovascular Research, UConn Health researchers show how removing a protein can prevent this, as well as heart attacks and strokes in humans.

Macrophages are huge white blood cells that scour our bodies for dangerous material and act as a sort of cleanup team. However, macrophages can cause problems in those who have atherosclerosis, which is characterized by fatty deposits and inflammation in the blood vessels. They eat too much fat inside artery walls, which causes them to froth up. Foamy macrophages can promote artery inflammation and can break away plaques, releasing clots that can lead to heart attacks, strokes, or embolisms elsewhere in the body.

According to a team of UConn Health researchers, changing how macrophages express a certain protein could avoid this type of harmful behavior. TRPM2 is a protein that is activated by inflammation, according to researchers. It instructs macrophages to begin consuming fat. TRPM2 is frequently triggered because blood vessel inflammation is one of the fundamental causes of atherosclerosis. TRPM2 activation increases macrophage activity, resulting in more foamy macrophages and possibly more inflamed arteries.

TRPM2’s ability to activate macrophages surprised Lixia Yue, a cell biologist at UConn School of Medicine.

“They form a vicious cycle promoting the development of atherosclerosis,” says Yue.

At least in mice, Yue and Pengyu Zong, a graduate student and the paper’s lead author, demonstrated one approach to break the loop. TRPM2 was knocked out of a lab mouse that is prone to atherosclerosis. The mice did not appear to be harmed by the deletion of that protein, and the macrophages did not become foamy. It also helped the animals with their atherosclerosis.

Yue and Pengyu Zong, as well as the rest of the team, are now investigating whether greater TRPM2 expression in blood monocytes (precursors to macrophages) correlates with the severity of cardiovascular disease in patients.

If they discover a correlation, elevated TRPM2 levels may serve as a predictive marker for heart attack and stroke.

Image Credit: Getty

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