Cardiovascular Research Advance Access originally published online on February 15, 2008
Cardiovascular Research 2008 78(1):5-7; doi:10.1093/cvr/cvn042
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.
Novel signalling cascade for cardiac hypertrophy activation by uncoupling and internalization of β1-adrenoceptors
Department of Cardiovascular Pharmacology, Yamagata University School of Medicine, 2-2-2 Iida-nishi, Yamagata 990-9585, Japan
* Corresponding author. Tel: +81 23 628 5234; fax: +81 236 28 5235. E-mail address: mendou@med.id.yamagata-u.ac.jp
| The first 10% of the full text of this article appears below. |
This editorial refers to Endocytosis machinery is required for b1-adrenergic receptor-induced hypertrophy in neonatal rat cardiac myocytes by Carmine Morisco et al.,11 pp. 36–44, this issue.
The immediate adaptation of cardiac pump function to haemodynamic stress is achieved by cardiac functional response, such as an increase in heart rate and cardiac contractility regulated through the Frank-Starling mechanism, the force-frequency relationship and adrenergic nerve stimulation. When the haemodynamic stress continues, cardiac hypertrophy develops first as the adaptive response of the myocardium that progresses to pathological (maladaptive) hypertrophy associated with fibrosis and apoptosis, and ultimately to heart failure. Maladaptive cardiac hypertrophy generally predisposes to heart failure and is an important risk factor for an increase in death of patients with heart failure, and therefore the signalling processes responsible for the development of cardiac hypertrophy have
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- Endocytosis machinery is required for β1-adrenergic receptor-induced hypertrophy in neonatal rat cardiac myocytes
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- Endocytosis machinery is required for β1-adrenergic receptor-induced hypertrophy in neonatal rat cardiac myocytes
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