Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adaptation, Physiological
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Animals
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Arrhythmias, Cardiac / etiology
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Arrhythmias, Cardiac / prevention & control
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Calcium / physiology
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Cardiac Output
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Cardiovascular Agents / therapeutic use*
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Cell Size
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Clinical Trials as Topic
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Heart Diseases / complications
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Heart Diseases / physiopathology
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Heart Failure / etiology
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Heart Failure / prevention & control
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Humans
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Hypertrophy, Left Ventricular / drug therapy*
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Hypertrophy, Left Ventricular / etiology
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Hypertrophy, Left Ventricular / metabolism
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Hypertrophy, Left Ventricular / physiopathology
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Ion Channels / physiology
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Mechanoreceptors / physiology
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Muscle Proteins / physiology
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Myocytes, Cardiac / metabolism
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Myocytes, Cardiac / pathology
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Pressure
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Ventricular Remodeling / drug effects
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Ventricular Remodeling / physiology
Substances
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Cardiovascular Agents
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Ion Channels
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Muscle Proteins
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Calcium