Heart failure is a serious and long-lasting condition that affects millions of people around the world.
It usually begins with heart muscle damage and when this happens, the heart becomes weaker and cannot pump blood as well as it should.
Over time, the heart struggles to send enough blood to the rest of the body, which leads to fatigue, shortness of breath, swelling in the legs, and many other problems that make daily life difficult.
Even though doctors have treatments that can ease symptoms and help patients live longer, there is still no cure that can stop the disease from progressing.
For decades, doctors have relied on the same medicines, and while these drugs help control blood pressure and reduce strain on the heart, they do not fix the underlying damage.
One of the biggest challenges in treating heart failure has been the lack of understanding about what truly drives the disease forward.
A research team from Penn State College of Medicine, led by Dr. Shyam Bansal, believes they may have uncovered an important piece of the puzzle.
Their work suggests that the body’s own immune system, which normally protects us from infections and helps heal injuries, may actually worsen heart failure over time.
The immune system is made up of many different types of cells that work together to keep the body healthy. Among them are helper T cells, a type of white blood cell that plays a key role in organizing immune responses.
These cells are usually helpful. They help the body fight viruses and bacteria, and they assist in healing wounds after injuries. Under normal conditions, helper T cells travel through the blood, lymph nodes, and spleen, ready to respond when something goes wrong.
Dr. Bansal became interested in helper T cells because of a simple but important question. If these cells can help heal a cut on the skin, why do they fail to repair damage in the heart after a heart attack?
In their new study, they examined heart tissue from healthy people and from patients with heart failure and studied closely how immune cells behave inside failing hearts.
In failing human hearts, helper T cells were far more active and more numerous than in healthy hearts. In particular, a group called CD4+ helper T cells stood out.
These cells were not only more active, but they were also multiplying at a higher rate. This level of immune activity suggested that inflammation was playing a much larger role in heart failure than previously thought.
The researchers also discovered that these CD4+ helper T cells showed increased activity in a signaling pathway linked to estrogen. When this pathway becomes too active, it can promote inflammation and scar tissue formation in the heart. Over time, this scarring contributes to worsening heart function.
Dr. Bansal and his team plan to continue studying these immune pathways to see whether new drugs can be developed to block the harmful immune response without weakening the body’s ability to fight infections.