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.
| Original language | English |
|---|---|
| Pages (from-to) | 373-380 |
| Number of pages | 8 |
| Journal | Cardiovascular Research |
| Volume | 63 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Aug 15 2004 |
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Keywords
- Left ventricular hypertrophy
- Pressure overload
- Signaling
- Transgenic mice
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Adaptive and maladaptive hypertrophic pathways : Points of convergence and divergence. / Selvetella, Giulio; Hirsch, Emilio; Notte, Antonella; Tarone, Guido; Lembo, Giuseppe.
In: Cardiovascular Research, Vol. 63, No. 3, 15.08.2004, p. 373-380.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Adaptive and maladaptive hypertrophic pathways
T2 - Points of convergence and divergence
AU - Selvetella, Giulio
AU - Hirsch, Emilio
AU - Notte, Antonella
AU - Tarone, Guido
AU - Lembo, Giuseppe
PY - 2004/8/15
Y1 - 2004/8/15
N2 - 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.
AB - 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.
KW - Left ventricular hypertrophy
KW - Pressure overload
KW - Signaling
KW - Transgenic mice
UR - http://www.scopus.com/inward/record.url?scp=3242774502&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3242774502&partnerID=8YFLogxK
U2 - 10.1016/j.cardiores.2004.04.031
DO - 10.1016/j.cardiores.2004.04.031
M3 - Article
C2 - 15276462
AN - SCOPUS:3242774502
VL - 63
SP - 373
EP - 380
JO - Cardiovascular Research
JF - Cardiovascular Research
SN - 0008-6363
IS - 3
ER -