Heart disease is still the number one cause of death in the United States. It includes serious problems like heart attacks and strokes.
Doctors have made great progress in fighting it over the years by treating high blood pressure, diabetes, and using medicines like aspirin and statins to lower cholesterol. But even with these tools, many people still develop heart disease. It’s like trying to put out a fire that keeps coming back.
Now, scientists at the University of Michigan may have found a missing piece of the puzzle—a protein in our bodies called suPAR. This protein might be one reason why heart disease is still so hard to stop.
SuPAR stands for “soluble urokinase plasminogen activator receptor.” It’s a protein made in the bone marrow, and it helps control the immune system. You can think of it like a thermostat that tells the immune system how active to be. But when suPAR levels get too high, things can go wrong. One of the major problems it may cause is atherosclerosis.
That’s a condition where arteries—the blood vessels that carry blood from the heart—become hard and narrow. This limits blood flow and can lead to heart attacks or strokes.
The researchers started by looking at data from over 5,000 people who didn’t have heart disease. They found that those with high suPAR levels were more likely to develop atherosclerosis later, even if they didn’t have other common risk factors like high cholesterol or diabetes.
Next, they studied the genes of 24,000 people. They discovered that some people have a version of a gene that causes them to make more suPAR. These people had higher levels of the protein in their blood.
When they checked an even bigger group of 500,000 people, they found that this gene version was linked to a higher risk of heart disease. They saw the same pattern in two other large databases, which makes the results even more convincing.
The team also studied mice. Mice that were given high levels of suPAR developed more fatty build-ups (called plaques) in their arteries than mice with normal levels. This means suPAR doesn’t just show up after a problem starts—it may be causing the problem in the first place.
This study is important because it pulls together different types of evidence—from human medical records, genetic data, and lab studies with animals—and they all point to the same conclusion: suPAR plays a major role in causing atherosclerosis.
Now, scientists are trying to find a way to lower suPAR levels safely. If they succeed, it could lead to a brand-new way to prevent and treat heart disease, especially for people who haven’t been helped by current treatments.
The researchers also found another interesting link. People with high suPAR levels were also more likely to have kidney disease. This makes sense, since about two-thirds of people with kidney disease also have heart disease, and many people with heart disease show signs of kidney problems. The same protein may be playing a harmful role in both.
This research was led by Dr. Salim Hayek and published in the Journal of Clinical Investigation. It reminds us how closely connected our organs are, and how one small part of the body—like a single protein—can have a big impact on our overall health. Understanding suPAR better could lead to life-saving treatments and a better future for people with heart and kidney diseases.
If you care about heart disease, please read studies about a big cause of heart failure, and common blood test could advance heart failure treatment.
For more information about heart health, please see recent studies about a new way to repair human heart, and results showing drinking coffee may help reduce heart failure risk.
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