© 1999 American Heart Association, Inc.
Point/Counterpoint |
Signaling in Myocardial Hypertrophy
Life After Calcineurin?
From the National Heart and Lung Institute (NHLI) Division, Imperial College School of Medicine, London, United Kingdom.
Correspondence to Peter H. Sugden, DPhil, NHLI Division (Cardiac Medicine), Imperial College School of Medicine, Dovehouse St, London SW3 6LY, United Kingdom. E-mail p.sugden@ic.ac.uk
Key Words: myocardial hypertrophy and failure • mitogen-activated protein kinase cascade • calcineurin • calcium movement • transcription
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Introduction |
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Cardiac (ventricular) hypertrophy is an important adaptive response in vivo that (at least in the shorter term) allows the organism to maintain or increase its cardiac output. Global ventricular hypertrophy is a recognized response to increased pressure or volume work (reviewed in Reference 11 ), with increased myofibrillogenesis and sarcomere deposition being cardinal features. Although global hypertrophy is clinically important, probably the most significant form of cardiac hypertrophy in terms of patient numbers is the localized hypertrophy of the ventricular wall that may follow loss of myocardium after a survivable myocardial infarct. In the early stages, both global and localized hypertrophy may resemble the readily reversible, nonfibrotic "physiological" hypertrophy that develops after repeated endurance exercise. In the longer term, beneficial, "compensated" hypertrophy may decay into maladaptive "decompensated" hypertrophy and heart failure (reviewed in References 2 and 32 3 ) with diminished coronary flow reserve and increased risk of lethal arrhythmias. Although some aspects of the maladapted state are probably intrinsic to the myocyte [eg, prolongation of the action potential and Ca2+ transient (reviewed in References 4 and 54 5 )], other factors (increased fibrosis and mismatch between O2 supply and demand) are also probably involved in decompensation.
The predominating view is that mammalian ventricular
myocytes lose their capacity for cell division during the perinatal
period and are thus terminally differentiated cells, although this is
still a matter of some dispute (reviewed in References 6 and 76 7 ). In
contrast, other cells in the heart (endothelial cells,
fibroblasts, and smooth muscle cells) retain
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