© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
Another activity for the cardiac biologist: CARP fishing
Internal Medicine 2, Intervet Pharma R&D S.A., Angers Technopole, Rue Olivier de Serres, BP 67131, Beaucouzé, France stephane.baudet@intervet.com
| The first 10% of the full text of this article appears below. |
See article by Zolk et al. [11] (pages 563–572) in this issue.
Despite several major advances in the management of congestive heart failure such as the introduction of angiotensin-converting enzyme inhibitors and beta-blockers, the prognosis of CHF remains poor and a major public health issue in westernised countries [1]. Accordingly, improved long-term pharmacological management of cardiac diseases will require new research characterised by basic work on the pathophysiology of the diseased cardiomyocyte.
Heart failure often results from long-term consequences of haemodynamic overload, which creates a mechanical stress on the cardiomyocytes. One of the earliest responses of the latter to this insult is reactivation of the foetal genes program, preceded by activation of transcription factors [2]. In most of these instances, reactivation of the foetal genes is transient and with no obvious link with the progressive deterioration of cardiac function.
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