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Cardiovascular Research 2001 50(1):7-9; doi:10.1016/S0008-6363(01)00234-6
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Signalling in cardiac disease: the molecular deficit at the heart of the problem

Terence E Hébert*

Centre de recherche, Institut de cardiologie de Montréal et Département d'anésthesie-réanimation, Université de Montréal, 5000 rue Bélanger est, Montreal, PQ, Canada, H1T 1C8

* Tel.: +1-514-376-3330; fax: +1-514-376-1355 hebertt@icm.umontreal.ca

Received 1 February 2001;

KEYWORDS G Protein; Signalling; Adrenergic receptors; Heart failure; Cardiomyocyte

The first 150 words of the full text of this article appear below.

See article by Yoshida et al. [3] (pages 34–45) in this issue.


   1 Introduction
 
Events leading to heart failure are characterized by a prolonged action potential and a deficit in cardiac performance which is paralleled by ionic remodelling and a loss of contractile function at the level of the single cardiomyocyte (see Ref. [1] for review). Increased sympathetic stimulation as well as a number of paracrine and autocrine factors lead to cardiac hypertrophy and an eventual decompensated failing phenotype [2]. However, several issues remain to be resolved in terms of a molecular mechanism for these events. First, is there a deficit in the contractile apparatus of the failing myocyte per se? Alternatively, are signalling pathways which modulate contractility and are known to be altered in the failing heart the trigger for these events? Further, the focus of work on whole cardiac tissue to date has not resolved the role of non-myocyte . . . [Full Text of this Article]


   2 Calcium-handling abnormalities
 

   3 Alterations in signal transduction pathways: what and where
 

   4 Questions remaining
 

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