Of the more than 700,000 Americans who suffer a heart attack each year, about a quarter go on to develop heart failure. Scientists don't fully understand how one condition leads to the other, but researchers in the Perelman School of Medicine at the University of Pennsylvania have now discovered a significant clue -- which ultimately could lead new therapies for preventing the condition.

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Heart failure can develop after a heart attack due to a long-term damage response by the immune system that transforms much of the heart muscle into stiff, fibrous, scar-like tissue. In a study published today in the Journal of Clinical Investigation, researchers report that a set of signaling proteins produced in the epicardium, a layer of special cells that lines the heart muscle, appears to play a key role in keeping this wayward damage-response process in check. "These findings highlight the importance of the heart's interaction with the immune system in the post-heart-attack response," said co-senior author Rajan Jain, MD, an assistant professor of Cardiovascular Medicine. "They hint at the possibility of developing designer therapies aimed at modulating specific aspects of immune system in the future as part of treating patients who have had a heart attack. "

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Prior work from Epstein and colleagues at Penn has shown that in the epicardium, a cascade of protein-to-protein interactions known as the Hippo signaling pathway occurs early in life and is important for normal heart development. Other research has suggested that two key components of the Hippo pathway, the signaling proteins YAP and TAZ, also promote the regeneration of heart muscle after experimental heart-attack-like damage in newborn mice. In this study, researchers examined the role of epicardial YAP and TAZ after heart attack in the adult heart, which, compared to the fetal or newborn heart, is much less able to regenerate itself following injury. After an experimentally induced heart attack, normal adult mice, as expected, showed a small amount of fibrous change in the heart, limited to the area where a coronary artery were blocked and heart muscle had been deprived of oxygen. By contrast, in adult mice whose YAP and TAZ genes had been deleted from their epicardial cells just before the heart attack, there were signs of widespread inflammation and fibrosis in the heart muscle.

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Source: https://www.sciencedaily.com/releases/2017/02/170207110923.htm
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