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Researchers have discovered that boosting levels of a tiny RNA in heart attack victims could greatly reduce heart muscle death over time.
After a heart attack, heart muscle can continue to die even when blood flow is restored, reducing the life expectancy of many people in recovery. However, new research has found that the addition of a tiny RNA into the heart can significantly reduce muscle death.
A research team from Augusta University has published a paper in the Journal of Molecular and Cellular Cardiology showing that in a mouse model, a human engineered version of the microRNA miR322 reduced heart muscle death by 40pc. The microRNA is known to coax stem cells to make heart cells during development, but in adult hearts their purpose remains unclear.
Using high throughput analysis of microRNAs, Dr Yaoliang Tang and his team were attempting to find better ways of protecting the heart from further damage. After determining that miR322 was the standout candidate, the team began looking for the source of it in adult hearts.
Eventually it was traced back to the endothelial cells that line blood vessels, and in the process found miR322’s target. In testing, the team caused an occlusion, or closure, in the left coronary artery of mice for about 45 minutes.
During the moment of the heart attack, the team saw reduced miR322 levels that recovered after blood and oxygen was restored. However, this dropped off dramatically just one day later, before reaching its lowest point seven days later.
An expensive fix
This is because while the heart is desperately seeking new blood and oxygen, many heart cells can find it hard to readjust and simply die.
When the manufactured miR322 was introduced, levels of the heart cell protector Notch 1 significantly increased while levels of cell suicide promoter FBXW7 significantly decreased, and heart damage reduced.
However, Tang noted that the half-life of miR322 is just a few seconds and is currently very expensive to produce, but one day it could be used in the immediate aftermath of a heart attack to reduce permanent heart damage.
Another option would be to find a way to bolster the body’s natural means of producing miR322, which the team is now looking into. It is also looking to do tests in larger animals models, in addition to learning more about two other microRNAs that seem to function as partners to miR322.
