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In the March issue of Nature Medicine, Jeffrey Molkentin and colleagues report a new strategy to treat heart disease by inhibiting the enzyme protein kinase C-alpha (PKC-alpha).
PKC-alpha is expressed at higher levels in heart failure patients, but the significance of this increase had not been well understood. Molkentin and colleagues used three mouse models of heart disease to show that deleting the gene that encodes PKC-alpha from the diseased heart improves its function. In two of the models, the technique helped the mice survive longer. The authors also show that PKC-alpha directly controls the activity of key enzymes that regulate heart muscle contraction. The authors' findings help explain the mechanisms behind heart muscle contraction, and suggest that PKC-alpha could be a pharmacologic target for treating human heart failure. Author contact: Jeffrey D. Molkentin
Children's Hospital Medical Center
Cincinnati, OH
USA
Tel: +1 513 636 3557
E-mail: jeff.molkentin@cchmc.org Abstract available online. (C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza
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