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Signaling in myocardial hypertrophy: life after calcineurin?

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 their mitotic capacity. Although ventricular myocytes are not the only cell type involved in the overall hypertrophic response, much of the ventricular enlargement or remodeling is attributable to their hypertrophy. The identities of signaling pathways that couple the demand for increased …