Heart disease remains the leading cause of death around the world and continues to place a huge burden on families and healthcare systems. Among the many forms of heart disease, coronary artery disease is the most common.
This condition develops when fatty deposits known as plaque build up inside the arteries that supply blood and oxygen to the heart. Over time, these deposits can narrow the arteries and reduce blood flow.
If a plaque suddenly breaks apart, it can trigger a heart attack or stroke. In the United States alone, coronary artery disease is responsible for about one in every four deaths, making it one of the most serious health problems facing modern society.
Although doctors have made major progress in treating heart disease through cholesterol-lowering medicines, blood pressure control, healthier lifestyles, and improved medical procedures, scientists are still trying to understand the deeper biological processes that cause the disease to develop and worsen.
A better understanding of these processes could lead to entirely new treatments that help prevent life-threatening events before they happen.
Now, researchers at the University of Virginia Health have uncovered an important clue that may help explain how heart disease progresses. Their findings, published in the journal Circulation: Genomic and Precision Medicine, focus on special cells found in the walls of blood vessels.
These cells, called smooth muscle cells, play an important role in keeping blood vessels healthy. Under normal conditions, they help maintain the structure and strength of artery walls. When plaque develops inside an artery, smooth muscle cells can move toward the plaque and form a protective covering known as a fibrous cap.
This cap acts like a shield that helps keep the plaque stable. Stable plaques are less likely to rupture and cause dangerous blood clots that can lead to heart attacks or strokes.
However, scientists have long been puzzled by the fact that these same cells do not always remain protective. In some cases, smooth muscle cells appear to change their behavior and begin contributing to plaque growth instead.
Rather than helping protect the artery, they may become part of the problem. Understanding why this transformation occurs has been a major question in cardiovascular research.
To investigate this mystery, doctoral student Noah Perry worked with smooth muscle cells collected from heart transplant donors. By examining the activity of genes inside these cells, he searched for biological pathways that might explain why the cells sometimes switch from helpful to harmful.
The study revealed that changes in the way cells handle nitrogen and store energy may play an important role.
In particular, the researchers found signs that problems involving glycogen, the stored form of sugar used by the body for energy, may be linked to the change in cell behavior. These findings suggest that the metabolism of smooth muscle cells could be much more important to heart disease than previously believed.
The researchers also identified another surprising factor: a naturally occurring sugar called mannose. Their results suggest that mannose may be involved in the process that causes smooth muscle cells to change their function. While the connection is still being investigated, the discovery provides an intriguing new direction for future studies.
The importance of this work lies in its potential medical applications. If scientists can determine exactly what triggers smooth muscle cells to become harmful, they may be able to develop treatments that prevent the change from happening. Such therapies could slow plaque growth, improve artery health, and reduce the risk of heart attacks and strokes.
Dr. Mete Civelek, who led the research team at the University of Virginia School of Medicine, noted that heart disease continues to affect millions of people worldwide despite significant advances in treatment. He believes that discovering new biological mechanisms behind the disease is essential for developing the next generation of therapies.
The study was carried out by a team that included Noah Perry, Diana Albarracin, and Redouane Aherrahrou. Their work adds an important piece to the growing understanding of how heart disease develops at the cellular level.
Although more research is needed before these findings can lead directly to new treatments, the discovery opens the door to promising possibilities.
Scientists often make progress by uncovering small details about how the body works, and those details can sometimes lead to major breakthroughs years later. This latest discovery highlights how understanding the behavior of individual cells may eventually help doctors better protect patients from one of the world’s deadliest diseases.
If you care about heart health, please read studies about top foods to love for a stronger heart, and why oranges may help fight obesity, diabetes, and heart disease.
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