According to a recent research, development of heart failure can be reduced especially in those who have already experienced at attack by enhancing the levels of a protein in the heart.//
S100A1 is the protein, whose level when increased above normal, helped in protecting animal hearts from added damage after simulated heart attacks. This was revealed by the study conducted by Cardiology researchers at the Center for Translational Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia.
In some cases, the animals' heart function hardly changed at all. At the same time, other animals with heart cells lacking the gene for the protein couldn't handle the stress of a heart blockage; they went on to develop heart failure.
The findings provide more evidence that falling levels of S100A1 are critical in the loss of heart-pumping strength after a heart attack and play an important role in the progression to heart failure. Potential therapeutic strategies, the researchers say, may focus on restoring S100A1 levels to normal. The work appears September 19, 2006, in the American Heart Association journal Circulation.
The researchers, led by Walter Koch, Ph.D., director of the Center for Translational Medicine in the Department of Medicine in Jefferson Medical College of Thomas Jefferson University in Philadelphia, examined two types of mice: transgenic mice which had extremely high levels of the gene for and the protein S100A1, and knockout mice that lacked S100A1 altogether.
S100A1, part of a larger family of proteins called S100, is primarily found at high levels in muscle, particularly the heart. Previous studies by other researchers showed that the protein was reduced by as much as 50 percent in patients with heart failure. Several years ago, Dr. Koch and his co-workers put the human gene that makes S100A1 into a mouse, and found a resulting increase in contractile strength of the heart cell. Page: 1 2 3 Related medicine news :1
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