Molecular mechanisms crucial for new approach to heart disease therapy mapped

ScienceDaily | 2/13/2018 | Staff
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In this study, published in Cell Reports, two labs at UNC and a group at Princeton University reprogrammed ordinary cells called fibroblasts into new and healthy heart muscle cells, and recorded changes that appear to be necessary for this reprogramming.

"From these studies we may be able to define pathways to increase the efficiency of fibroblast reprogramming," said senior author Frank Conlon, PhD, professor of genetics in the UNC School of Medicine and professor of biology in the UNC College of Arts and Sciences.

Heart - Disease - People - Year - United

Heart disease kills more than 600,000 people each year in the United States alone and remains the leading cause of death for both men and women. It typically arises from the narrowing or blockage of coronary arteries and involves the progressive replacement of heart muscle cells (cardiomyocytes) with scar tissue -- leading to a loss of heart function and ultimately heart failure.

This progressive disease process occurs in part because cardiomyocytes have a very limited ability to proliferate and replace damaged heart muscle. Scientists therefore have been experimenting with techniques to transform fibroblasts -- collagen-making cells that are abundant in the heart -- into new cardiomyocytes. They have shown that they can make this therapeutic cell-reprogramming process work in the diseased hearts of lab mice and thereby improve heart function. But the process isn't as efficient as it needs to be for clinical use, and scientists are still learning why.

Application - Technology - Lack - Understanding - Mechanisms

"The application of this technology has been limited by our lack of understanding of the molecular mechanisms driving this direct reprogramming process," said Conlon, who is also a member of the UNC McAllister Heart Institute.

For this study, Conlon's lab -- in collaboration with...
(Excerpt) Read more at: ScienceDaily
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