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Cardiovascular Research 2001 49(1):7-10; doi:10.1016/S0008-6363(00)00273-X
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Nucleoside diphosphate kinase: a new player in heart failure?

Ying-Ying Zhou and Michael Artman*

Pediatric Cardiology, TWR Suite 9-V, NYU Medical Center, 540 First Avenue, New York, NY 10016, USA

* Corresponding author. Tel.: +1-212-263-5993; fax: +1-212-263-5808 michael.artman@med.nyu.edu

Received 30 October 2000; accepted 30 October 2000

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

See article by Lutz et al. [33] (pages 48–55) in this issue.

Despite considerable efforts, the incidence, prevalence and mortality of heart failure remain high in most industrialized countries [1,2]. This is partially due to the complex nature of the heart failure syndrome. As a final outcome of many types of heart disease, the degree of heart failure varies from case to case depending on the pathological history, genetic basis and environmental background. However, the most common feature of the failing heart is diminished systolic and/or diastolic function, associated with disturbed intracellular Ca2+ homeostasis. Under physiological conditions, cardiac contraction is initiated by Ca2+ influx through sarcolemmal L-type Ca2+ channels, which subsequently triggers a large amount of Ca2+ release from the internal sarcoplasmic reticulum (SR) stores via ryanodine receptors. The increased intracellular Ca2+ activates the contractile myofilaments, and then is either recycled back into the SR by SR Ca2+ pumps . . . [Full Text of this Article]


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