Hypertrophy of the heart: a new therapeutic target?
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.
Frey
Norbert
N
Department of Cardiology, University of Heidelberg (N.F., H.A.K.), Heidelberg, Germany.
Katus
Hugo A
HA
Olson
Eric N
EN
Hill
Joseph A
JA
D000222:Adaptation, Physiological; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000517:prevention & control; D002118:Calcium / Q000502:physiology; D002302:Cardiac Output; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D048429:Cell Size; D002986:Clinical Trials as Topic; D006331:Heart Diseases / Q000150:complications / Q000503:physiopathology; D006333:Heart Failure / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D007473:Ion Channels / Q000502:physiology; D008465:Mechanoreceptors / Q000502:physiology; D009124:Muscle Proteins / Q000502:physiology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D011312:Pressure; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology
D002317:Cardiovascular Agents; D007473:Ion Channels; D009124:Muscle Proteins; D002118:Calcium