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Cardiovascular Research 2000 47(1):4-5; doi:10.1016/S0008-6363(00)00077-8
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

A depressing future for cyclosporine?

Virginia J Owen*

National Heart and Lung Institute at Imperial College School of Medicine, Dovehouse Street, London SW3 6LY, UK

* Tel.: +44-207-351-8173; fax: +44-207-376-3442 v.j.owen@ic.ac.uk

Received 15 March 2000; accepted 20 March 2000

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

See article by Janssen et al. [1] (pages 99–107) in this issue.

In this issue of the journal, Janssen and colleagues [1] examine the in vitro effects of cyclosporine A (CsA) on myocardial contractile function in multi-cellular preparations obtained from human and rabbit hearts.

The effect of CsA on cardiac muscle function is currently highly fashionable following the recent flurry of data concerning its effect on the phosphatase calcineurin in the progression of cardiac muscle hypertrophy [2]. CsA bound to its major binding protein, cyclophilin A, forms a complex that inhibits the phosphatase activity of calcineurin and, in turn, blocks dephosphorylation of the transcription factor NF-AT3 (for review, see [3]). The current paper by Janssen, in conjunction with other published data, provides us . . . [Full Text of this Article]


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