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MIAMI – Despite decades of research and prevention and treatment methods, heart disease remains the leading cause of death in the U.S. and other countries.

For decades, medical care has focused on controlling well-known risk factors such as high blood pressure, high cholesterol, diabetes, smoking, and obesity.

Medicines including statins and aspirin, together with healthier lifestyles, have saved countless lives.

However, many people still develop heart attacks and strokes despite having these traditional risk factors under good control. This has led scientists to search for other hidden causes of heart disease.

A new study from researchers at the University of Michigan has uncovered an important clue.

According to Knowridge, the team discovered that an immune system protein called soluble urokinase plasminogen activator receptor, or suPAR, may play a direct role in causing heart disease.

The researchers focused on a condition called atherosclerosis, which is the main cause of most heart attacks and strokes.

Atherosclerosis develops when fatty deposits, cholesterol, and other substances slowly build up inside the walls of arteries.

Over time, these deposits form plaques that narrow and harden the arteries, reducing blood flow.

If a plaque suddenly breaks open, it can trigger a blood clot that blocks blood flow to the heart or brain, researchers said.

Scientists have known for many years that high cholesterol and high blood pressure increase the risk of atherosclerosis.

However, these factors do not explain every case.

The new research suggests that ongoing inflammation caused by high levels of suPAR may be another important reason why arteries become damaged.

SuPAR is produced mainly by cells in the bone marrow as part of the body’s immune system. Normally, the immune system protects us from infections and helps repair injuries.

But when suPAR levels remain high for a long time, the immune system stays constantly active. This persistent inflammation can slowly damage blood vessels and make plaque more likely to form inside arteries.

To investigate this idea, the researchers first studied more than 5,000 adults who had no known heart disease.

They found that people with higher suPAR levels were much more likely to develop atherosclerosis later, even when their cholesterol levels and blood pressure were normal.

The scientists then examined the genetic information of about 24,000 people.

They discovered that a gene called PLAUR helps control how much suPAR the body produces. People who carried certain versions of this gene tended to have higher suPAR levels and a greater risk of developing heart disease.

To strengthen the evidence, the researchers used a powerful research method called Mendelian randomization. This approach uses naturally occurring genetic differences to test whether one factor actually causes another.

Using health data from about 500,000 people in the United Kingdom, the team found strong evidence that high suPAR levels do not simply occur alongside heart disease—they help cause it.

The researchers also performed experiments in mice. Animals with high suPAR levels developed much more severe plaque buildup in their arteries than mice with normal levels. These laboratory results supported what was seen in the human studies.

The discovery is especially important because today’s standard heart medicines do not reduce suPAR levels. Drugs such as statins are very effective at lowering cholesterol, but they do not target this immune protein.

Researchers are now working to develop treatments that can lower suPAR, which could provide extra protection for people who remain at high risk despite receiving the best available care.

The study also offers new insight into the close connection between heart disease and chronic kidney disease. Previous research has linked high suPAR levels to kidney damage. If future medicines can safely reduce this protein, they may help protect both the heart and the kidneys at the same time.

Although more research and clinical trials are still needed, this discovery could change the way doctors think about heart disease.

Instead of focusing only on cholesterol and blood pressure, future treatments may also target harmful inflammation caused by suPAR.

If successful, this new approach could help reduce heart attacks and strokes for millions of people around the world.