Coronary artery disease is one of the most common forms of heart disease and a major cause of death.
It develops when fatty material, cholesterol and other substances collect inside the arteries that supply blood to the heart. These deposits, known as plaques, can narrow the arteries and make it harder for the heart muscle to receive enough oxygen.
If a plaque becomes unstable and breaks open, a blood clot can form and suddenly block blood flow.
This can cause a heart attack and, in some cases, other serious cardiovascular problems. Scientists are therefore trying to understand not only why plaques form, but also what makes some plaques more dangerous than others.
Researchers at University of Virginia Health have uncovered new clues involving smooth muscle cells in artery walls. These cells normally help blood vessels keep their shape and control how wide or narrow they become.
They can also help create a strong covering over artery plaques, which may make the plaques less likely to rupture.
But smooth muscle cells are surprisingly flexible. During coronary artery disease, some can change their behavior and take on different roles. Certain changes may help protect an artery, while others may encourage plaque growth and inflammation.
This has created an important question for heart researchers: what tells these cells to change from a helpful state into one that may worsen disease? A team led by Dr. Mete Civelek, working with doctoral researcher Noah Perry and colleagues, looked for answers by studying smooth muscle cells obtained from heart transplant donors.
The researchers examined differences in gene activity and the chemical processes that cells use to survive and function. Their results pointed to an unexpected connection involving nitrogen metabolism and glycogen metabolism. Glycogen is a stored form of sugar that cells can break down when they need energy.
The findings suggest that changes in these metabolic pathways may influence how artery smooth muscle cells behave.
In other words, the way a cell processes nutrients and other molecules may help determine whether it remains protective or shifts toward a state linked with plaque development. This could reveal new biological targets for future heart treatments.
The researchers also identified mannose as a molecule of interest. Mannose is a simple sugar that is naturally present in the body and is involved in several cell processes. The study suggests it may be connected with harmful changes in smooth muscle cells, although scientists still need to determine exactly what role it plays.
This work is important because current heart treatments do not eliminate all cardiovascular risk. Medicines that lower cholesterol or blood pressure can greatly reduce the chance of heart attack and other complications, but people can still develop coronary artery disease.
Finding additional processes that drive plaque formation could eventually lead to treatments that work alongside existing medicines.
However, the discovery does not mean people should try to change their mannose intake or use supplements based on these results.
The research is aimed at understanding what happens inside artery cells, and much more work is needed before the findings can be turned into a treatment. Future studies will need to confirm how these pathways affect plaque development in the human body.
For now, well-established ways to reduce coronary artery disease risk remain important. These include not smoking, staying physically active, eating a heart-healthy diet, controlling blood pressure and cholesterol, maintaining a healthy weight and managing diabetes when present.
People at higher risk can also work with their doctors to decide whether medication is needed.
The study by the University of Virginia Health team, including Perry, Diana Albarracin, Redouane Aherrahrou and Civelek, was published in the journal Circulation: Genomic and Precision Medicine.
By revealing more about the unusual behavior of smooth muscle cells, the research may help scientists develop new ways to prevent dangerous artery plaques in the future.
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