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Cardiovascular Research 2001 49(2):249-252; doi:10.1016/S0008-6363(00)00275-3
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Adenovirus gene transfer of SERCA in heart failure. A promising therapeutic approach ?

A Baartscheer*

Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE, Amsterdam, The Netherlands

* Tel.: +31-20-566-3265; fax: +31-20-697-5458 a.baartscheer@amc.uva.nl

Received 30 October 2000; accepted 30 October 2000

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

See article by Chossat et al. [10] (pages 288–297) in this issue.


   1 Introduction
 
Abnormal and reduced contractile function is characteristic in patients suffering from heart failure. Therefore, it seems obvious that inotropic therapy could potentially be beneficial in the treatment of heart failure. However, a number of studies show short-term beneficial effects with progressive myocardial dysfunction in long-term treatment with inotropic interventions in chronic heart failure [1,2]. Inotropic interventions not only enhance contractility and cytosolic systole calcium concentration ([Ca2+]), but also potentially adversely affect diastolic [Ca2+].

Functional abnormalities commonly observed in the failing heart include a negative force frequency relationship secondary to disturbed calcium handling [3–6] characterized by increased diastolic [Ca2+], increased duration and reduced amplitude of the calcium transient and reduction of the SR calcium content [7,8]. Available evidence strongly suggests that down regulation of the sarcoplasmic reticular SR Ca-ATPase (SERCA) underlies these abnormalities possibly . . . [Full Text of this Article]


   2 Present limitation of adenoviral SERCA gene transfer
 

   3 Metabolic and electrophysiological effects of up-regulation of SERCA
 
3.1 Metabolic effects
3.2 Electrophysiological effects

   4 Concluding remark
 

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