CHAPEL HILL, N.C. After a heart attack, the portions of the heart damaged by a lack of oxygen become scar tissue. Researchers have long sought ways to avoid this scarring, which can harden the walls of the heart, lessen its ability to pump blood throughout the body and eventually lead to heart failure. But new research from the University of North Carolina at Chapel Hill School of Medicine shows that interrupting this process can weaken heart function even further.
In a study appearing online November 15, 2011, in the EMBO Journal, the investigators observed that cells in the outer layer of the heart generated scar tissue. But when they blocked these cells from doing so, they essentially demonstrated that when fixing a broken heart, timing may be everything.
"We now know that scarring is a good thing, because it prevents a precipitous decline in heart function immediately after heart injury," said Arjun Deb, MD, senior study author and assistant professor of medicine and cell and molecular physiology at the UNC School of Medicine. "The question is not whether, but when it makes the most sense to manipulate the cells of the heart to decrease scarring and enhance regeneration." Deb is also a member of UNC's McAllister Heart Institute and the Lineberger Comprehensive Cancer Center.
Regeneration happens naturally in lower organisms like zebrafish the striped, thumb-sized inhabitants of household aquariums but for some reason not in higher organisms like humans. Years ago researchers noticed that a thin outer layer of cells on the surface of the heart muscle known as the epicardium was playing an important role in regenerating the zebrafish heart after injury. But what role the epicardium might have in an injured mammalian heart was an open question.
By studying a mouse model of cardiac injury, Deb and his colleagues found that the epicardium of the mammalian heart was also activated after a heart attack. But un
|Contact: Les Lang|
University of North Carolina School of Medicine