When a person has a heart attack, portions of the heart muscle die in the next several days or even weeks if deprived of oxygen for long enough. The recovering heart slowly remodels itself, even fostering the growth of new blood vessels, in an attempt to regain some of its former function. But all too often, the remodeling is actually harmful, and the damaged heart is on an inevitable downward slide to heart failure. Now, scientists at the Center for Translational Medicine at Temple University School of Medicine have identified a key target they hope will help stave off the potentially harmful effects of remodeling. They have shown that by turning off the activity of a protein, GSK-3a, in the heart cells of mice that have had a heart attack, they can prevent heart remodeling, preserve heart function and significantly improve survival.
