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Cardiovascular Research 2004 62(3):447-449; doi:10.1016/j.cardiores.2004.03.021
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Adenosine receptors, heart rate, and cardioprotection

Matteo E Mangoni* and Stéphanie Barrère-Lemaire

Laboratoire de Génomique Fonctionnelle (LGF), CNRS UPR 2580, IGH CNRS UPR 1142; 141 rue de la Cardonille, Montpellier, Cedex 5, France

* Corresponding author. Tel.: +33-4-99-61-99-39; fax: +33-4-99-61-99-01. Email address: matteo.mangoni@igh.cnrs.fr

Received 15 March 2004; accepted 22 March 2004

The first 10% of the full text of this article appears below.

See article by Fabritz et al. [1] (pages 500-508) in this issue.

In this issue of Cardiovascular Research, a paper by Fabritz et al. [1] investigates the effects of controlled overexpression of the A3 adenosine receptor (A3AR) in the mouse heart. Their findings will feed further the current debate on the use of adenosine receptors (AR) as targets for gene therapy aimed at protecting the myocardium against ischemic damage. Furthermore, Fabritz et al. report interesting observations on the functional role of adenosine receptors in the regulation of heart rate.


   1. Adenosine and cardioprotection
 
In the heart, adenosine regulates pacemaker activity as well as different cellular functions through the A1, A2, and A3AR. ARs are expressed on different cell types, including myocytes, vascular and endothelial cells, fibroblasts, and neutrophils (for review, see Ref. [2]). . . . [Full Text of this Article]


   2. Gene therapy and AR
 

   3. Perspectives for the study of heart rate regulation
 

   4. Conclusions
 

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