One-quarter of all Americans who have a heart attack go on to experience heart failure, and researchers from the University of Pennsylvania have uncovered a new clue as to why.
After a heart attack, your immune system may elicit a long-term damage response that results in the heart muscle becoming stiff, fibrous, and scar-like. Researchers now contribute this to signaling proteins in the epicardium—a layer of cells that lines the heart and has been found to play a role in moderating this damage response. Previous research has shown that two proteins in the epicardium, YAP and TAZ, encourage the regeneration of the heart muscle.
In this most recent study, the role of these proteins after a heart attack was examined in mice. Regular adult mice showed a small amount of fibrous change in the heart, though it was limited to the region that had been deprived of oxygen during the attack.
Researchers compared these results to those from mice who had their YAP and TAZ genes deleted, and saw that the mice without the regenerative proteins experienced extensive inflammation and fibrosis, rather than just localized fibrous change. Dr. Rajan Jain aided in the research and commented, “The hearts of these mice were essentially encased in fibrotic cells. We found that this extreme fibrotic response was accompanied by a decline in heart function resembling what is seen in human heart failure, as well as rapid weight loss and a much higher death rate.”
The results of this study show a connection between the presence of YAP and TAZ and the ability for the heart to regenerate itself after heart attack damage. The team hopes that this new understanding will provide scientists with new therapeutic targets to help prevent heart attack patients from developing heart failure.
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