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Heart size and function uncoupled by researchers

t PI3K gamma, we had normal heart size and much better function. With both of these proteins shut down, we had huge hearts and much better function. When we took out PI3K alpha, the mice had tiny hearts but normal function, and when we took out both PTEN and PI3K alpha, the mice had tiny hearts and heart failure. With these genes we can determine heart size and can genetically control how well our hearts pump, irrespective of the heart being normal or enlarged."

According to the World Health Organization, cardiovascular disease will be the most common cause of death within 20 years. This research goes directly to helping alleviate this disease, the researchers say. Every patient with heart or cardiovascular disease goes through a stage of heart enlargement. Those with hypertension, for example, need their heart to pump and contract more; as a result, the heart muscle enlarges to compensate for the extra work. At a certain point, however, this compensation doesn't work anymore and the heart starts to fail.

The scientists hope that this research will form the basis for better treatments for people with chronic heart failure or cardiovascular disease. "The problem now is that there is no drug which maintains the pumping function of the heart," says Penninger. "We found the proteins that genetically control this. So the hope is that if you can shut down PI3K gamma, the heart will function much better after a heart attack or chronic heart failure, even if the patient has an enlarged heart."


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Contact: Janet Wong
jf.wong@utoronto.ca
416-978-5949
University of Toronto
19-Sep-2002


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