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Cardiovascular Research 2000 48(2):191-193; doi:10.1016/S0008-6363(00)00207-8
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Sarcoplasmic reticulum calcium release function and FK binding proteins in heart failure: another piece of a complex jigsaw

Cesare M.N Terracciano*

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

* Tel.: +44-20-7352-8121, ext. 3322; fax: +44-20-7351-8145 c.terracciano@ic.ac.uk

Received 16 August 2000; accepted 16 August 2000

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

See article by Ono et al. [1] (pages 323–331) in this issue.

Dysfunction is a complex phenomenon in heart failure. Most cardiac structures are altered and functional relationships are disrupted. A global picture of the pathophysiology of heart failure is not yet available. However, many studies showing modifications of different aspects of cardiac physiology have been carried out and more pieces of this complex jigsaw are revealed. Amongst these, the paper by Ono et al., published in the present issue of Cardiovascular Research [1], focuses on the role of FK binding proteins (FKBPs) in heart failure.

FKBPs are immunophilin proteins associated with the SR Ca release channel (ryanodine receptor (RYR)), which have attracted attention because of their possible involvement in the pathophysiology of cardiac muscle. It has been suggested that, in muscle, FKBP stabilizes RYR function and this could be involved in the gating of the RYR [2,3]. . . . [Full Text of this Article]


   1 FKBP and SR Ca release function: the macromolecular complex
 

   2 SR Ca release and cytoplasmic Ca regulation: functional consequences for contraction
 

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