Experimental mRNA therapy promotes repair after heart attack damage

Scientists have devised a treatment that revives heart muscle cells to aid in repairing damage caused by heart attacks. In a study involving mice, this therapy resulted in a stronger heartbeat and a 10% increase in the volume of blood pumped by the heart with each contraction, compared to mice that received a placebo after experiencing a heart attack.

Although this is not a definitive cure, even minor enhancements to heart function have been associated with reduced mortality and improved daily functioning for patients. The treatment employs mRNA therapy to temporarily activate two proteins inside heart cells, known as Myc and Cyclin T1, which promote the repair of heart tissue.

This approach holds promise for treating patients with heart failure in the future. Heart failure affects approximately 200,000 individuals in the U.K. annually, and while existing treatments can alleviate symptoms and slow the progression of heart disease, they cannot regenerate heart muscle that has already been lost. Dr. Catherine Wilson, a co-senior author of the study from the University of Cambridge's Department of Pharmacology and Gurdon Institute, expressed excitement, stating, "There's no cure for heart failure, and our treatment could potentially have a meaningful impact on the quality of life for millions of people worldwide."

The research team is now focusing on refining the treatment, conducting further trials in larger animal models, and eventually in humans to fully assess its safety and efficacy. The findings were published in the journal Nature Cardiovascular Research. Following a heart attack, the mRNA therapy was administered to the hearts of the mice, and its effectiveness was evaluated using echocardiograms—similar to ultrasound examinations of a fetus in the womb.

Due to the short-lived and localized nature of the treatment, it is not anticipated to cause any permanent alterations to the heart cells, aiming to minimize the risk of uncontrolled growth. No adverse effects were observed in the mice during or after the treatment. After 28 days and 12 weeks, reassessing the mice revealed that the improvement in heart function was long-lasting.

An adult human heart can lose up to 1 billion heart muscle cells following a heart attack. Unlike most other organs in the body, the adult heart lacks the ability to regenerate lost cells, leading to reduced heart strength, scar formation, heart failure, and ultimately death. As the global population expands and the prevalence of heart failure rises, the cost of patient care is projected to surge significantly.

Researchers believe that reviving heart muscle cells through this method is a promising strategy for treating heart failure patients. Bryan Williams, chief scientific and medical officer at the British Heart Foundation, emphasized, "Reviving the human heart to repair itself is the ultimate goal for cardiologists. The heart readily repairs when we are babies in the womb, but shortly after birth, our heart muscle cells lose the ability to regenerate and mend the heart.

This makes it exhilarating to see studies like these reignite regeneration in heart muscle cells." While the research has been conducted in mice and is still in its early stages, it represents a significant step forward in developing therapies that could potentially repair heart damage following a heart attack. The study, titled "Transient modified mRNA encoding Myc and Cyclin T1 improves cardiac function after myocardial injury," was published in Nature Cardiovascular Research (DOI: 10.1038/s44161-026-00910-7).