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Updated 10:00 AM October 12, 2009
 

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  Research
Scientists jump-start heart cells by gene transfer

Scientists from U-M and Minnesota show that gene therapy may be used to improve an ailing heart's ability to contract properly.

In addition to showing gene therapy's potential for reversing the course of heart failure, it also offers a glimpse of a day when "closed heart surgery" via gene therapy is as commonly prescribed as a cocktail of drugs.

"We hope that our study will lead some day to the development of new genetic-based therapies for heart failure patients," says Todd Herron, research assistant professor of molecular and integrative physiology. "The advent of molecular motor-based gene transfer for the failing heart will hopefully improve cardiac function and quality of life for heart failure patients."

Herron and colleagues treated heart muscle cells from the failing hearts of rabbits and humans with a virus (adenovirus) modified to carry a gene that produces a protein that enables heart cells to contract normally (fast molecular motor) or a gene that becomes active in failing hearts, which is believed to be part of the body's way of coping with its perilous situation (slow molecular motor). Heart cells treated with the gene to express the fast molecular motor contracted better, while those treated with the gene to express the slow molecular motor were unaffected.

"Helping hearts heal themselves, rather than prescribing yet another drug to sustain a failing organ, would be a major advance for doctors and patients alike," says Dr. Gerald Weissmann, editor-in-chief of the FASEB Journal, in which the results were reported. "Equally important, it shows that gene therapy remains one of the most promising approaches to treating the world's most common and deadliest diseases."

The most common causes of heart failure are coronary artery disease, hypertension or high blood pressure, and diabetes. Current treatments usually involve 3-4 medicines: ACE inhibitors, diuretics, digoxin and beta blockers.

Current clinical agents and treatments focus on the amount of calcium available for contraction, which can provide short-term cardiac benefits, but are associated with increased mortality in the long-term. This study shows that calcium-independent treatments could have implications for heart diseases associated with depressed heart function, due to the effectiveness of fast molecular motor gene transfer on the improved contractions of human heart muscle cells.

Other U-M authors include Eric Devaney, associate professor of cardiac surgery; Lakshmi Mundada, research laboratory specialist in molecular and integrative physiology; Sharlene Day, assistant professor of internal medicine; Guadalupe Guerrero-Serna, research fellow in internal medicine; Margaret Westfall, associate professor of surgery and molecular and integrative physiology; and Joseph Metzger, University of Minnesota, and U-M adjunct professor of molecular and integrative physiology.

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