Heart disease, a leading cause of death in Western countries, often refers to a condition called atherosclerosis. This disease is characterized by the buildup of plaque in arteries, which narrows them and restricts the flow of oxygen-rich blood.
Plaque is made up of cholesterol, fatty materials, calcium, and other biological debris. Over time, this buildup can harden and lead to serious complications like heart attacks and strokes.
For years, the dominant explanation for atherosclerosis has been the Lipid Hypothesis, also known as the Cholesterol Hypothesis. This theory links high cholesterol levels directly to plaque formation and narrowed arteries.
However, new research from New York University suggests there’s more to the story—platelets, tiny fragments in the blood that are essential for clotting, may play a significant role in triggering artery-damaging inflammation.
Platelets are typically known for their role in stopping bleeding by forming clots at injury sites. But the study revealed that platelets also contribute to inflammation, which is central to the development of atherosclerosis.
When activated, platelets release substances that attract white blood cells (leukocytes) to inflamed areas of blood vessels. This process, called chemotaxis, involves leukocytes moving toward high-inflammation regions, where they adhere to and penetrate the blood vessel walls.
The researchers also identified a specific protein called SOCS3, which appears to be influenced by platelets and is linked to the progression of atherosclerosis. SOCS3 was found to play a role in platelet-mediated inflammation, particularly in myeloid cells (a type of white blood cell). This interaction accelerates plaque formation in arteries, even in the absence of blood clots.
Interestingly, the study showed that this inflammatory process is not necessarily connected to thrombosis, the clot formation commonly associated with heart attacks. Instead, the findings suggest that platelets have a separate role in promoting inflammation that contributes to heart disease.
Further evidence came from patients studied in the research. Women who had heart attacks showed elevated levels of SOCS3 protein and increased activity in monocyte-platelet aggregates (clusters of white blood cells and platelets).
Another group of patients with atherosclerosis in their leg arteries also had higher levels of SOCS3, more active platelets, and signs of inflammation. These findings establish a direct link between platelet-driven inflammation, SOCS3 protein, and heart disease.
This research highlights a new perspective on how atherosclerosis develops, emphasizing the importance of platelets in triggering and sustaining inflammation. While cholesterol remains a key factor in heart disease, understanding the inflammatory role of platelets may open doors to new treatments targeting inflammation rather than just cholesterol levels.
For individuals at risk of heart disease, this study underscores the importance of managing both cholesterol and inflammation. Lifestyle changes, such as a healthy diet, regular exercise, and stress reduction, remain essential, alongside medical interventions as recommended by healthcare providers.
The study, led by Dr. Tessa Barrett and her team, was published in Science Translational Medicine, adding crucial insights into the complex mechanisms behind heart disease.
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