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Jefferson scientists use gene therapy to restore function of damaged heart cells in lab

Researchers at Jefferson Medical College and Duke University have used gene therapy to help damaged heart cells regain strength and beat normally again in the laboratory. The work takes the scientists one step closer to eventual clinical trials in humans.

Walter Koch, Ph.D., director of the Center for Translational Medicine of the Department of Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia, and his colleagues at Duke used a virus to carry a gene into the heart cells of individuals who had suffered from congestive heart failure. The gene introduced into these heart cells blocks the activity of an enzyme that is increased in failing human hearts and which contributes to the loss of the heart's contractile strength during the development of heart failure. When the activity of this enzyme is blocked by the gene therapy, the heart cells were able to contract at normal strength and their overall performance was improved.

Dr. Koch and his co-workers at Duke University Medical Center in Durham, N.C., report their findings April 6, 2004, in Circulation, a journal of the American Heart Association.

According to Dr. Koch, who is W.W. Smith Professor of Medicine at Jefferson Medical College of Thomas Jefferson University, researchers have known for some time that the beta-adrenergic receptor system fails to work properly in individuals with congestive heart failure. Such receptors "drive the heart both by rate and force of contraction," he says.

The researchers' target has been the beta-adrenergic kinase (ARK1), an enzyme that is elevated in human heart failure. One of its functions is to turn off beta-adrenergic receptors. "In heart failure, beta adrenergic receptor density is decreased, ARK is increased and both together cause dysfunctional beta receptor signaling," Dr. Koch says. "A failing heart then has little capacity to respond to exercise or stress because there are fewer receptors and the remaining rec
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5-Apr-2004


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