Myocardial hypertrophy is a response of cardiac muscle to altered conditions of haemodynamic overload caused by a large number of physiological and pathological conditions. Traditionally, it has been considered a beneficial mechanism. However, sustained hypertrophy has been associated with a significant increase in the risk of cardiovascular disease and mortality. Actually, many researchers are trying to understand whether left ventricular hypertrophy is a 'good' mechanism to stimulate or a 'bad' process to prevent. In this review we investigate the most common biochemical signaling pathways involved in the hypertrophic response to identify the precise role, either 'adaptive' or 'maladaptive', of each molecular pathway. Delinealing intracellular signaling pathways involved in the different aspects of cardiac hypertrophy will permit future improvements in the signaling that controls beneficial growth.

Adaptive and maladaptive hypertrophic pathways: points of convergence and divergence

HIRSCH, Emilio;TARONE, Guido;
2004

Abstract

Myocardial hypertrophy is a response of cardiac muscle to altered conditions of haemodynamic overload caused by a large number of physiological and pathological conditions. Traditionally, it has been considered a beneficial mechanism. However, sustained hypertrophy has been associated with a significant increase in the risk of cardiovascular disease and mortality. Actually, many researchers are trying to understand whether left ventricular hypertrophy is a 'good' mechanism to stimulate or a 'bad' process to prevent. In this review we investigate the most common biochemical signaling pathways involved in the hypertrophic response to identify the precise role, either 'adaptive' or 'maladaptive', of each molecular pathway. Delinealing intracellular signaling pathways involved in the different aspects of cardiac hypertrophy will permit future improvements in the signaling that controls beneficial growth.
63
373
380
http://cardiovascres.oxfordjournals.org/cgi/reprint/63/3/373
Left ventricular hypertrophy; Signaling; Transgenic mice; Pressure overload
G. SELVETELLA; E. HIRSCH; A. NOTTE; G. TARONE; G. LEMBO
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2318/36668
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