A recent study from New York University has found that platelets, the tiny fragments in our blood that help with clotting, also play a major role in inflammation that damages arteries. This discovery sheds light on how heart disease develops beyond just cholesterol buildup.
Heart disease, particularly atherosclerosis, is one of the leading causes of death in Western countries. It happens when fatty deposits, cholesterol, and other substances build up inside arteries, forming plaque. Over time, this plaque hardens and narrows the arteries, making it harder for oxygen-rich blood to flow. This can lead to heart attacks and strokes.
For many years, scientists have focused on cholesterol as the main cause of atherosclerosis. This idea, known as the Cholesterol Hypothesis, suggests that high cholesterol leads to plaque buildup. However, researchers now believe there is more to the story.
The new study, published in Science Translational Medicine, shows that platelets also play a critical role in this process by triggering inflammation.
Platelets are usually known for their job in blood clotting. When you get a cut, they stick together to form a clot and stop the bleeding. But this study found that platelets do much more. They release substances that attract white blood cells (also called leukocytes) to areas of inflammation in the arteries. This reaction, in turn, speeds up plaque formation.
The researchers also found that platelets affect a protein called SOCS3. This protein influences how the body responds to inflammation. The study showed that platelets help regulate SOCS3 in a way that makes atherosclerosis worse. This means platelets not only contribute to plaque buildup but also drive the inflammation that damages arteries.
Interestingly, while platelets are involved in inflammation and plaque formation, they do not always cause thrombosis—the process of forming dangerous blood clots inside arteries. Instead, they contribute to heart disease in a different way, by promoting long-term artery damage.
The researchers looked at different groups of patients and found a clear connection between platelets, inflammation, and heart disease. In women who had heart attacks, there was an increase in SOCS3 protein levels and more platelets stuck to white blood cells.
Another group of patients with atherosclerosis in their legs also had high SOCS3 levels, more active platelets, and more inflammation.
These findings provide new evidence that platelets are not just passive clotting agents but active players in heart disease. Understanding their role in inflammation could lead to new ways to prevent or treat atherosclerosis, beyond just focusing on cholesterol.
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