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Cardiovascular Research 2003 57(2):294-297; doi:10.1016/S0008-6363(02)00825-8
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Human heart failure: our current STATus of knowledge

Vanessa P.M van Empel and Leon J De Windt*

Hubrecht Laboratory, Royal Netherlands Academy of Sciences and Arts, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands

* Corresponding author. Tel.: +31-30-212-1800; fax: +31-30-351-6464. dewindt@niob.knaw.nl

Received 21 November 2002; accepted 25 November 2002

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

See article by Ng et al. [10] (pages 333–346) in this issue.

Is this a dagger which I see before me ... or art Thou but a dagger of the mind ... From Shakespeare's Macbeth (II, I, 33).


   1. gp130/STAT signaling and human heart failure
 
Cardiac muscle hypertrophy involves the exuberant growth of individual myofibers triggered by increased mechanical load (as in chronic hypertensive disease) or decreased mechanical performance (as observed in ischemic damage) and constitutes an independent clinical risk factor for heart failure development [1,2]. Consequently, elucidating the molecular circuitry controlling the initiation and maintenance of cardiac remodeling is the focus of intense research in modern cardiovascular biology. Integrative approaches have identified dozens of ligands, receptors, cytoplasmic signal amplifiers and transcriptional effectors of myocyte hypertrophy in the last decade [3]. Nevertheless, the challenge remains to identify those common disease-provoking and -sustaining pathways, given the variability in genetic susceptibility and environmental disparities of general human . . . [Full Text of this Article]


   2. Cardiac signaling: the good, the bad and where STAT may fit in
 

   3. gp130 signaling: inherent negative feedback signals
 

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