Heart disease remains the leading cause of death in the United States and many other countries. It causes heart attacks, strokes, and heart failure, claiming millions of lives each year.
Doctors have reduced the risk for many people by treating high blood pressure, high cholesterol, diabetes, and other well-known risk factors, but many cardiovascular events still occur despite these treatments.
Researchers have long suspected that other causes of heart disease have yet to be discovered. A new study from the University of Michigan points to one possible missing piece. The researchers found strong evidence that an immune system protein called suPAR may directly contribute to the buildup of fatty plaques inside arteries.
When fatty deposits collect in the walls of arteries, the condition is known as atherosclerosis. Over time, these plaques narrow and harden the arteries, making it harder for blood to flow. If a plaque suddenly breaks open, it can trigger a blood clot that blocks blood flow to the heart or brain, causing a heart attack or stroke.
The protein studied by the researchers is called soluble urokinase plasminogen activator receptor, or suPAR. It is produced mainly in the bone marrow and helps regulate immune activity.
Previous studies had shown that people with high suPAR levels were more likely to develop heart disease, but scientists did not know whether the protein actually caused the disease or was simply a warning sign.
To answer this question, the research team analyzed health information from more than 5,000 adults who did not already have heart disease. They found that people with higher suPAR levels were more likely to develop atherosclerosis, even if they had normal cholesterol levels and normal blood pressure. This suggested that suPAR could be an independent risk factor.
The researchers then studied the genes of about 24,000 people. They identified a variation in a gene called PLAUR, which controls how much suPAR the body produces. People carrying this genetic variation had higher suPAR levels and were also more likely to develop atherosclerosis.
To strengthen the findings, the team examined genetic information from about 500,000 participants in the UK Biobank. They found the same connection between higher suPAR levels and heart disease. Two additional large studies produced similar results, adding further support to the discovery.
The scientists also carried out experiments in mice. Animals with higher levels of suPAR developed much larger artery plaques than mice with normal levels. These experiments suggested that suPAR is not simply associated with heart disease but may actively help drive the disease process.
The discovery could open the door to new treatments. Current medicines, such as statins, mainly lower cholesterol but do not target suPAR. Researchers are now working on therapies that could safely reduce suPAR levels, which may provide another way to prevent or slow atherosclerosis.
The study may also help explain why heart disease and kidney disease often occur together. High suPAR levels have previously been linked to kidney damage, suggesting that the same immune protein could contribute to both conditions. Understanding this connection may lead to better treatments for patients affected by both diseases.
The study was led by Dr. Salim Hayek and colleagues at the University of Michigan and published in the Journal of Clinical Investigation. The findings suggest that inflammation and the immune system play a much larger role in heart disease than previously understood.
Although more research is needed before new treatments become available, targeting suPAR could eventually provide a new way to prevent heart attacks and strokes, especially for people whose risk cannot be fully explained by cholesterol or blood pressure alone.
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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