Experimental mRNA therapy promotes repair after heart attack damage
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Scientists have developed a treatment that 'reawakens' heart muscle cells so they start to divide and help repair damaged muscle.
In a study in mice, this produced a stronger heartbeat and increased the amount of blood pumped through the heart with each heartbeat by around 10%, compared with mice that received a mock treatment, following a heart attack.
While this is not a full cure, even small improvements to heart function have been linked to lower mortality in patients and a better ability to carry out daily activities.
The treatment uses mRNA therapy to temporarily activate two proteins inside heart cells, called Myc and Cyclin T1, promoting repair of heart tissue.
This has the potential in the future to be used to treat patients with heart failure. Around 200,000 people in the U.K. are diagnosed with heart failure each year, and while current treatments can reduce symptoms and slow the progression of heart disease, they can't regenerate heart muscle that has already been lost.
"These are really exciting results. There's no cure for heart failure, and our treatment could potentially have a meaningful impact on the quality of life of millions of people around the world," said Dr. Catherine Wilson, associate professor at the University of Cambridge's Department of Pharmacology and Gurdon Institute, co-senior author of the study.
She added, "We're not just treating the symptoms of heart failure—this approach could help the heart to repair itself."
The team is now working to refine the treatment. Further trials in larger animal models, and then in humans, are needed to fully establish its safety and effectiveness.
The results are published in the journal Nature Cardiovascular Research.
Testing the treatment
Following a heart attack, the mRNA therapy was injected into the hearts of the mice and its effectiveness assessed by looking at the hearts with an echocardiogram—similar to looking at a baby inside the womb.
Since the treatment is short-lived and localized, it is not expected to cause any permanent modification to the heart cells—an approach designed to reduce the risk of overgrowth. No adverse effects were seen in the mice.
Reassessing the mice after 28 days and after 12 weeks showed that the improvement in heart function is long-lasting.
Can we teach the heart to heal itself?
After a heart attack, an adult human heart can lose up to 1 billion heart muscle cells. Unlike many other organs in the body, the adult heart can't regenerate itself, so lost cells are never replaced. Their loss reduces the strength of the heart and can lead to scar formation, heart failure and ultimately death.
As the world's population grows and the prevalence of heart failure increases, the cost of patient care is anticipated to increase dramatically. The scientists believe that reawakening heart muscle cells in this way is a promising approach to treating heart failure patients.
Bryan Williams, chief scientific and medical officer at the British Heart Foundation, said, "Getting the human heart to repair itself is the holy grail for cardiologists. The heart is easily repaired when we are babies in the womb, but our heart muscle cells lose the ability to regenerate and fix the heart shortly after we are born.
"That makes it exciting when studies like this are able to reignite regeneration in heart muscle cells. The gene therapy used by the researchers shows clear potential for heart patients. While the research is in mice, and still at an early stage, it is an important step forward toward therapies which could help repair the damage to the heart following a heart attack."
Publication details
A transient modified mRNA encoding Myc and Cyclin T1 improves cardiac function after myocardial injury, Nature Cardiovascular Research (2026). DOI: 10.1038/s44161-026-00910-7.
Journal information: Nature Cardiovascular Research
Key medical concepts
Myocytes, CardiacMyocardial infarctionMYC Family Protein
Clinical categories
CardiologyClinical pharmacology Provided by University of Cambridge Who's behind this story?
Gaby Clark
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