Heart failure is a serious condition that affects millions of people. It happens when the heart muscle becomes weak or damaged, often after a heart attack. The heart can no longer pump enough blood to meet the body’s needs.
Over time, this leads to a drop in heart function, sometimes to below 40%. In the United States alone, about 6.7 million adults over the age of 20 live with heart failure, according to the Centers for Disease Control and Prevention.
Sadly, nearly half of these patients die within five years of diagnosis. There is currently no cure to stop the condition from getting worse.
For many years, doctors have used the same kinds of medications to manage heart failure. While these treatments can help control symptoms, they do not stop the disease from progressing. One reason may be that scientists do not fully understand what causes the heart to continue failing over time.
A new study from Penn State College of Medicine offers a new explanation. The research team, led by Associate Professor Shyam Bansal, has discovered that the body’s own immune system may be making things worse.
Specifically, a type of immune cell called helper T cells, which are normally helpful in fighting infections and healing wounds, appear to become overactive in hearts with heart failure. Instead of helping, they may be causing more damage.
This is the first time that such T cell activity has been directly seen in human hearts. The researchers believe this discovery could change the way we think about heart failure. By identifying the immune system’s role, they hope to create new treatments that target these harmful cells.
Helper T cells usually move around the body in the blood or live in the lymph nodes and spleen. When there is an injury, like a cut or an infection, they come in to help start the healing process. Bansal wondered why these cells could help repair skin wounds but fail to repair damage in the heart.
In earlier studies using mice, Bansal’s team found that these T cells are helpful right after a heart attack. But later, during long-term heart failure, the same cells seem to switch roles and start harming the heart instead of healing it.
In the new study, the researchers examined heart tissue samples from both healthy and failing human hearts. They also used public data to support their findings. What they found was that helper T cells—specifically a type called CD4+ T cells—were much more active in failing hearts than in healthy ones.
These overactive T cells also showed increased activity in a cell-signaling pathway linked to estrogen. This kind of signaling, when too strong, is known to cause scarring and inflammation in the heart.
Both of these problems are connected to poor heart function. In earlier research, Bansal’s group had already linked this same estrogen signaling to worsening heart failure in mice.
While it’s still not completely clear what exact role these CD4+ T cells play, the findings suggest that heart failure might involve an autoimmune response. In other words, the immune system may mistakenly attack the heart as if it were a threat. This is a new way of thinking about the disease.
Bansal and his team plan to continue their research. They want to find out if blocking these harmful immune pathways can stop the damage and slow down the disease. If they succeed, it could lead to new treatments that target inflammation and immune cells instead of just focusing on the heart itself.
This discovery brings hope to millions of people living with heart failure. By better understanding how the immune system affects the heart, researchers may one day develop more effective ways to treat this deadly condition.
If you care about heart health, please read studies that yogurt may help lower the death risks in heart disease, and coconut sugar could help reduce artery stiffness.
For more information about health, please see recent studies that Vitamin D deficiency can increase heart disease risk, and results showing vitamin B6 linked to lower death risk in heart disease.
The study is published in Journal of Molecular and Cellular Cardiology.
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