It's Not Just Cholesterol That Clogs Arteries

Researchers have discovered a gene that is directly linked to the development of cardiovascular diseases, such as high blood pressure and diabetes, and that acts independently of cholesterol levels.

Cardiovascular disease tops the list of the most common causes of death globally. Until now, treating cardiovascular disease has primarily revolved around lowering cholesterol levels. However, as researchers at the Washington University School of Medicine in St. Louis discovered, it’s not just blood lipid levels that are causative factors; genes play a central role as well.

The team, led by cardiologist Nathan O. Stitziel, studied genetic data and used experimental animal models of atherosclerosis (or the formation of arterial plaques) to investigate the genetic factors at play in this condition. They discovered a gene called SVEP1 is a major player. SVEP1 codes for an inflammatory protein that accelerates the development of arterial plaques. Mice lacking one copy of the gene showed less arterial clogging and reduced the risk of atherosclerosis.

The researchers also observed that SVEP1 spiked inflammation in the artery walls, making the plaques more prone to breaking loose—a phenomenon that can result in a heart attack or stroke.

“In animal models, we found that the protein-induced atherosclerosis and promoted unstable plaque,” said In-Hyuk Jung, co-first author of the study, published in ScienceTranslational Medicine. “We also saw that it increased the number of inflammatory immune cells in the plaque and decreased collagen, which serves a stabilizing function in plaques.”

This discovery paves the way for a novel therapeutic approach for minimizing the risk of coronary artery disease. SVEP1 was active during early embryonic development, but eliminating the protein in adult mice did not appear to have any detrimental consequences.

Given this observation, the researchers hypothesize that therapeutically altering SVEP1 levels could pose a promising and safe way of managing cardiovascular disease in high-risk patients.

Sources: Washington University in St. Louis, Science Translational Medicine.