Heart disease is a term that encompasses a range of complex conditions, with atherosclerosis being one of the most prominent.
Atherosclerosis, a condition marked by the accumulation of plaque in arteries, is a leading cause of death in Western countries.
This plaque consists of cholesterol, fatty substances, calcium deposits, and various biological debris. Over time, this plaque hardens and narrows the arteries, restricting the flow of oxygen-rich blood.
The prevailing theory, known as the Lipid Hypothesis or Cholesterol Hypothesis, attributes atherosclerosis to high cholesterol levels. However, this hypothesis doesn’t tell the whole story of how plaque forms and contributes to heart attacks and strokes.
Recent research from New York University has unveiled a crucial piece of the puzzle.
Platelets, tiny cellular fragments with a primary role in blood clot formation, were found to trigger a harmful inflammatory response in the arteries. Platelets are essential for clotting blood at injury sites to stop bleeding.
In the study, scientists explored the role of platelets in atherosclerosis development.
They discovered that platelets have functions beyond their role in preventing excessive bleeding. These small, sticky fragments also play a significant role in inflammation and plaque formation.
Activated platelets were found to release a multitude of inflammatory substances that facilitate the movement, adhesion, and passage of immune cells (leukocytes) to areas of inflammation within blood vessels.
This process, known as chemotaxis, is instrumental in the inflammatory response.
The researchers also identified that platelets have an impact on a protein called SOCS3. They found that platelet-mediated regulation of myeloid SOCS3 accelerates atherosclerosis development.
It’s important to note that while platelets are integral to atherosclerosis development, they are not solely involved in thrombosis—clot formation in arteries. Instead, they contribute significantly to the inflammation process.
The study further revealed that among women who had experienced heart attacks, there was an increase in the SOCS3 protein along with heightened monocyte-platelet aggregates.
In a separate group of patients with atherosclerosis in their leg vessels, elevated SOCS3 proteins, increased platelet activity, and inflammation were observed.
These findings establish a causal connection between platelet-mediated myeloid inflammation, SOCS3, and heart disease.
For those concerned about inflammation, it’s worth exploring studies that link vitamin D deficiency to chronic inflammation and the potential benefits of vitamin B in reducing inflammation and combating COVID-19.
For additional information on inflammation, recent research offers insights into innovative methods to curb excessive inflammation and dietary approaches that may help reduce inflammation in COVID-19 cases.
In conclusion, the research conducted by Dr. Tessa Barrett and her team, published in Science Translational Medicine, has uncovered a pivotal role for platelets in the development of heart disease.
This discovery goes beyond the traditional focus on cholesterol and highlights platelets’ involvement in inflammation, offering new avenues for understanding and addressing this prevalent health issue.
If you care about heart health, please read studies about the best time to take vitamins to prevent heart disease, and scientists find how COVID-19 damages the heart.
For more information about heart health, please see recent studies about Aspirin linked to higher risk of heart failure, and results showing this drug could reduce heart disease, fatty liver, obesity.
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