A mouse heart treated with an experimental therapy pumped about 10% more blood with each beat than a heart given a mock treatment. The improvement lasted for at least 12 weeks in the University of Cambridge study, offering a promising clue in the search for ways to help damaged hearts repair themselves.
A heart attack can destroy large numbers of heart muscle cells. In adults, the heart does not replace these lost cells, which can leave weaker muscle and scar tissue behind. That damage can lead to heart failure, a condition in which the heart cannot pump blood as well as the body needs. Current treatments can ease symptoms and slow the disease, but they cannot bring back heart muscle that has already been lost.
The Cambridge team tested an mRNA treatment in mice after a heart attack. Messenger RNA, or mRNA, carries temporary instructions that tell cells to make certain proteins. In this case, the treatment briefly activated two proteins in heart cells: Myc and Cyclin T1. The researchers found that this encouraged heart muscle cells to divide, a process that could help repair injured tissue.
The therapy was injected into the mice’s hearts. The team used an echocardiogram, a scan that shows how the heart is working, to measure its effect. Treated mice pumped around 10% more blood per heartbeat than mice given the mock treatment. When the researchers checked again after 28 days and 12 weeks, the improvement in heart function was still there.
The treatment was designed to act only for a short time and in a limited area, rather than permanently changing heart cells. That may help reduce the risk of uncontrolled cell growth. The researchers reported no adverse effects in the mice, but the early result does not establish that the approach is safe or effective in people. The team says it needs to refine the treatment and test it in larger animals before human trials can be considered.
Even a modest gain in heart function could matter. The source article notes that small improvements have been linked to lower mortality and a greater ability to manage everyday activities. About 200,000 people in the United Kingdom are diagnosed with heart failure each year, and the number of people living with the condition is expected to grow as populations age and expand.
Dr. Catherine Wilson, associate professor at the University of Cambridge’s Department of Pharmacology and Gurdon Institute and a co-senior author, said the approach might help the heart repair itself rather than only treat symptoms. Bryan Williams, chief scientific and medical officer at the British Heart Foundation, described heart repair as a major goal for cardiologists, while stressing that the research remains at an early stage and has so far been tested in mice.
The findings, published in Nature Cardiovascular Research, do not yet offer a treatment for patients. But they give researchers a specific next step: find out whether temporarily prompting heart cells to divide can be made safe and useful beyond the mouse heart.