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Cardiovascular Research 2004 63(3):367-372; doi:10.1016/j.cardiores.2004.06.012
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Synchronization and integration of multiple hypertrophic pathways in the heart

Klaus-Dieter Schlüter*,a and Kai C Wollertb

aPhysiologisches Institut, Universität Giessen, Aulweg 129, 35392 Giessen, Germany
bAbteilung Kardiologie und Angiologie, Medizinische Hochschule Hannover, Carl-Neuberg Str. 1, 30625 Hannover, Germany

* Corresponding author. Tel.: +49-641-99-47-212; fax: +49-641-99-47-219. Email address: klaus-dieter.schlueter@physiologie.med.uni-giessen.de

Received 9 June 2004; accepted 16 June 2004

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

Nine years ago, Cardiovascular Research (vol. 30(4), 1995) published a Spotlight Issue on signal transduction summarizing important cellular signaling events in cardiovascular cells. At that time, a main focus of research was centered on intracellular cascades modifying cellular responses in multiple cardiovascular cells, including vascular smooth muscle cells, cardiac fibroblasts, and cardiomyocytes. The present Spotlight Issue is intended to give the readership of Cardiovascular Research an update on the aforementioned signaling cascades involved in myocardial hypertrophy and to point out what has become increasingly evident during the last decade: multiple hypertrophic pathways work together in a complex scenario by integration and synchronization of a multitude of signals generated by distinct mechanisms. This editorial briefly introduces the topics covered in this Spotlight Issue.


   1. Definitions
 
Epidemiological evidence from the Framingham study identifies myocardial hypertrophy that occurs in pathological conditions of chronically increased workload (e.g. hypertension, valvular heart disease, myocardial infarction) as a risk . . . [Full Text of this Article]


   2. Example 1: neurohumoral factors
 

   3. Example 2: the renin–angiotensin system
 

   4. Example 3: cross-talk between hypertrophic and vasodilatory factors
 

   5. Outlook
 

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