(Circulation. 2004;109:1580-1589.)
© 2004 American Heart Association, Inc.
Review: Current Perspective |
From the Department of Cardiology (Innere Medizin III), University of Heidelberg (N.F., H.A.K.), Heidelberg, Germany, and Departments of Molecular Biology (E.N.O., J.A.H.) and Internal Medicine (J.A.H.) and the Donald W. Reynolds Cardiovascular Clinical Research Center (E.N.O., J.A.H.), University of Texas Southwestern Medical Center, Dallas, Tex.
Correspondence to Joseph A. Hill, MD, PhD, Cardiology Division, Department of Internal Medicine, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8573. E-mail joseph.hill{at}UTsouthwestern.edu
Recent studies call into question the necessity of hypertrophic growth of the heart as a "compensatory" response to hemodynamic stress. These findings, coupled with recent progress in dissecting the molecular bases of hypertrophy, raise the prospect of suppressing hypertrophy without provoking circulatory insufficiency. In this article, we focus on signaling pathways that hold promise as potential targets for therapeutic intervention. We also summarize observations from animal models and clinical trials that suggest benefit from an antihypertrophic strategy.
Key Words: hypertrophy heart failure signal transduction
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