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Researchers at FSU Medical College are developing new possibilities to prevent sudden cardiac death

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In the United States, nearly 500,000 people die each year from sudden cardiac death (SCD) as a result of a malfunction of the heart’s electrical system.

The main cause of SCD in young athletes is arrhythmogenic cardiomyopathy (ACM). It is a hereditary disease in which a healthy heart muscle replaces scar tissue (fibrosis) and fat over time.

Stephen Cerco, an assistant professor of biomedical sciences at Florida State University School of Medicine, has developed a better understanding of the pathological features behind the disease and promising means for prevention. His findings are published in the latest issue of Science Translational Medicine.

Some people with ACM have mutations that cause arrhythmias. Arrhythmias are usually not fatal if properly managed and treated. However, Cerco shows that exercise not only amplifies these arrhythmias, but also causes widespread cell death. Their only option is to avoid participating in exercise, which should be a healthy and valuable endeavor.

“The exercise is terribly ironic, and what is known as a heart health benefit leads to cell death in ACM subjects,” Cerco said. “We now know that endurance exercise in particular leads to massive myocyte death due to mitochondrial dysfunction in people suffering from this hereditary heart disease.”

Thousands of mitochondria are present in almost every cell in the body, processing oxygen and converting food into energy. It is believed to be the driving force of all cells (they produce 90% of the energy our body needs to function properly) and also plays another important role as a protective antioxidant. I will.

When mitochondria do not function properly and the muscle cells of the heart die, healthy muscle is replaced by scar tissue and fat cells. Eventually, the normal electrical signal of the heart is reduced to the irregular and chaotic firing of impulses from the lower chamber, which prevents proper blood pumping during strenuous exercise. Without immediate treatment, death can occur within minutes.

Cerco’s research is at the heart of the processes involved in mitochondrial dysfunction.

“Ultimately, mitochondria are overwhelmed, driving out the’death signal’that is sent to the nucleus and initiating massive DNA fragmentation and cell death,” Cerco said. “This new study elucidates the pathogenic role of exercise-induced mitochondrial-mediated cell death in the ACM heart.”

In addition to providing a better understanding of the processes involved, Cerco found that cell death can be prevented by inhibiting two different mitochondrial proteins. One such approach utilizes a new targeting peptide developed for Chelco’s research by the National Research Council in Padua, Italy.

Its findings pave the way for the development of new treatment options to prevent myocyte death, cardiac dysfunction, and pathological progression with fatal consequences for people living with ACM.

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