The discovery identifies targets for the discovery of new drugs that could improve the quality of life in people suffering from chronic illness who could benefit from aerobic exercise, but are unable to perform the amount of exercise necessary to produce the desired effects, said R. Sanders Williams, M.D., dean of the Duke University School of Medicine and senior author of the study that appears in the April 12, 2002 issue of the journal Science. Drugs that stimulate this pathway also could reproduce health benefits of exercise that help to prevent diabetes and cardiovascular disease.

The research was conducted at UT Southwestern where Williams was director of the Ryburn Center for Molecular Cardiology until 2001 when he became dean of the School of Medicine at Duke.

In 1998, Williams and colleagues published findings showing that activating the signaling protein calcineurin could mimic some of the effects of endurance exercise. In the new study, which was funded by grants from the National Institutes of Health, researchers detail the discovery of another cellular signaling pathway involving a different class of signaling proteins called calmodulin-dependent protein kinases (CaMK) that controls genes that influence the physiological and metabolic properties of muscles.

"We think this discovery could lead to the synthesis of new drugs that will allow individuals to acquire the health benefits of regular exercise, even if they cannot exercise. It has the potential to improve the lives of patients with heart failure, pulmonary disease, renal failure, diabetes and other chronic diseases," Williams said.

Williams and his colleagues have spent 20 years studying why muscle tissues remodel themse
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Contact: Amy Reyes
a.reyes@duke.edu
919-668-7837
Duke University Medical Center
10-Apr-2002