The study showed that cholesterol accumulation is not the sole factor in this process; rather, the metabolic programming of immune cells, specifically phagocytes , plays a pivotal role in determining whether plaques will remain stable or progress to a more serious condition. It was found that these cells, when exposed to changes in their metabolic environment, enter a state of abnormal activity that affects the metabolism of lipids and amino acids.
Analysis of phagocytic cell activity in blood vessel walls, fatty tissue, and the liver revealed that the development of atherosclerosis is associated with the emergence of a distinctive metabolic pattern, characterized by increased activity of molecules such as Trem2, Folr2, and Slc7a7 , which are indicators reflecting profound shifts in the function of immune cells and the way they interact with fats within the vessel wall.
The researchers focused particularly on the amino acid transporter Slc7a7 , which is associated with glutamine metabolism. Experiments showed that disabling this protein reduces the ability of phagocytic cells to absorb modified fats and limits their transformation into what are known as "foam cells," which are the main component of atherosclerotic plaques.
The researchers suggest that these findings could change the traditional understanding of plaque formation, as it is not only linked to high blood lipid levels but also to how immune cells process nutrients. This discovery opens new avenues for developing more accurate diagnostic tools and innovative treatments to prevent cardiovascular disease.
The study was published in the journal Cardiovascular Research
