Cell Help After Heart Attack?
Cell Help After Heart Attack?
Cell Transplants Curb Life-Threatening Heart Rhythm After Heart Attack in Mice
Dec. 5, 2007 -- Scientists say they've found a new way to help prevent a dangerous, abnormal heart rhythm after a heart attack.
Heart attack damage can cause abnormal heart rhythms, which can be life-threatening.
Researchers in Germany and the U.S. have come up with a new way to curb a risky heart rhythm called ventricular tachycardia after a heart attack.
The method -- which has been tested in mice but not in people -- involves three steps:
Among mice that had had a heart attack, ventricular tachycardia was rarer in those that received the tweaked, transplanted cells than those that didn't get such cells.
Connexin 43 was the key, report the researchers, who included Wilhelm Roell, MD, of Germany's University of Bonn.
Roell's team noticed connexin 43 in experiments that involved heart cells from mouse embryos. Genetic engineering allowed adult muscle cells to make connexin 43 without involving embryos.
The study "represents a promising therapeutic strategy to decrease the risk of potentially fatal arrhythmias," Roell and colleagues write in tomorrow's edition of Nature.
Cell Help After Heart Attack?
Cell Transplants Curb Life-Threatening Heart Rhythm After Heart Attack in Mice
Dec. 5, 2007 -- Scientists say they've found a new way to help prevent a dangerous, abnormal heart rhythm after a heart attack.
Heart attack damage can cause abnormal heart rhythms, which can be life-threatening.
Researchers in Germany and the U.S. have come up with a new way to curb a risky heart rhythm called ventricular tachycardia after a heart attack.
The method -- which has been tested in mice but not in people -- involves three steps:
- Taking certain muscle cells from the mice (but not from the mice's heart muscle)
- Tweaking those cells to produce a protein called connexin 43
- Injecting the tweaked muscle cells into the mice's hearts
Among mice that had had a heart attack, ventricular tachycardia was rarer in those that received the tweaked, transplanted cells than those that didn't get such cells.
Connexin 43 was the key, report the researchers, who included Wilhelm Roell, MD, of Germany's University of Bonn.
Roell's team noticed connexin 43 in experiments that involved heart cells from mouse embryos. Genetic engineering allowed adult muscle cells to make connexin 43 without involving embryos.
The study "represents a promising therapeutic strategy to decrease the risk of potentially fatal arrhythmias," Roell and colleagues write in tomorrow's edition of Nature.
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