Heart disease remains the leading cause of death across the world. In the United States alone, it is responsible for about one out of every four deaths.
One of the most common and dangerous forms is coronary artery disease. This condition develops when fatty deposits, known as plaque, slowly build up inside the arteries that supply blood to the heart.
As the plaque grows, the arteries become narrower, making it harder for oxygen-rich blood to reach the heart muscle. If the plaque suddenly breaks open, a blood clot can form and block blood flow completely, causing a heart attack. Similar blockages in blood vessels leading to the brain can also cause a stroke.
Although doctors have made great progress in treating heart disease with medicines, surgery, and healthier lifestyles, coronary artery disease continues to affect millions of people every year. Researchers are therefore searching for new ways to better understand how the disease begins and why it becomes worse over time.
A new study from the University of Virginia Health has uncovered an unexpected clue. The research suggests that certain cells inside blood vessel walls may change their behavior and help the disease progress instead of protecting the heart. The findings were published in the journal Circulation: Genomic and Precision Medicine.
Healthy arteries are made of several layers. One important layer contains smooth muscle cells. These cells help blood vessels stay strong, flexible, and able to expand or tighten as blood flows through them. They also help form a protective covering over plaque. This covering acts like a shield that keeps plaque stable and lowers the chance that it will break apart.
For many years, scientists believed these smooth muscle cells mainly played a protective role. However, newer studies have shown that the cells can sometimes change into a harmful state.
Instead of helping repair blood vessels, they may encourage plaque to grow and make coronary artery disease more severe. Exactly why these cells change has remained a mystery.
To investigate this question, researchers led by Dr. Mete Civelek and graduate student Noah Perry studied smooth muscle cells collected from heart transplant donors.
They carefully examined the genes inside these cells to identify which ones might control their behavior. Looking at genes helps scientists understand how cells function and why they sometimes act differently under disease conditions.
The team discovered evidence linking these changes to the way the cells process nitrogen and glycogen. Glycogen is a form of stored sugar that the body keeps as an energy reserve.
Normally, cells carefully control how they use and store this energy. The researchers believe that when these processes become disrupted, the smooth muscle cells may begin changing into a harmful form that supports plaque growth instead of preventing it.
One sugar called mannose attracted particular attention during the study. Mannose is a naturally occurring sugar found in the body and in some foods. The researchers believe it may play a role in the changes seen in smooth muscle cells.
However, they stress that much more research is needed before scientists know exactly how mannose influences heart disease or whether it could become a treatment target.
This discovery is important because it opens a completely new direction for heart disease research. Most current treatments focus on lowering cholesterol, reducing blood pressure, preventing blood clots, or encouraging healthier lifestyles.
These treatments save many lives, but they cannot completely stop coronary artery disease from developing. If researchers can learn what causes smooth muscle cells to switch from helpful to harmful, they may be able to design medicines that stop this process before serious damage occurs.
Dr. Civelek explained that identifying new treatment targets is essential because heart disease remains a major health challenge despite existing therapies.
His research team, including Noah Perry, Diana Albarracin, and Redouane Aherrahrou, plans to continue studying these cell changes to better understand how they affect the development of coronary artery disease.
While scientists continue their work, there are many proven ways people can lower their own risk of heart disease. Eating plenty of fruits, vegetables, whole grains, and healthy fats, staying physically active, avoiding smoking, maintaining a healthy weight, getting enough sleep, and controlling blood pressure, cholesterol, and diabetes all help protect the heart.
Some studies also suggest that vitamin D may help reduce inflammation, while vitamin K has been linked with a lower risk of heart disease, although people should always talk with their healthcare provider before taking supplements.
The new findings offer another reminder that heart disease is more complex than once believed. By learning how individual cells change inside blood vessels, scientists hope to develop more effective treatments that prevent plaque from becoming dangerous.
Although more studies are needed before these discoveries can be turned into new medicines, the research provides an encouraging step toward better protection against one of the world’s deadliest diseases.
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