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Cardiovascular Research 2002 55(1):16-24; doi:10.1016/S0008-6363(02)00221-3
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

The wnt-frizzled cascade in cardiovascular disease

Marielle E. van Gijna, Mat J.A.P. Daemenb, Jos F.M. Smitsa and W.Matthijs Blankesteijna,*

aDepartment of Pharmacology, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands
bDepartment of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands

* Corresponding author. Tel.: +31-43-388-1417; fax: +31-43-388-4149 wm.blankesteijn@farmaco.unimaas.nl

Received 22 June 2001; accepted 17 December 2001

KEYWORDS Angiogenesis; Developmental biology; Infarction; Signal transduction

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


    1. Introduction
 
Wnt-proteins constitute a family of secreted cystein-rich glycosylated proteins, involved in a variety of modeling and remodeling processes including cell proliferation, differentiation, apoptosis and the control of cell orientation [1–3]. Malfunctioning of the wnt-frizzled pathway has been implied in diseases as divergent as cancer and Alzheimer's disease [1,4]. The wnt-frizzled signal transduction pathway plays an important role during non-vertebrate and vertebrate development [5]. Several studies have shown the importance of wnts in the control of processes such as patterning of the body axis and development of the central nervous system and the limbs [6,7]. Moreover, interventions in wnt signaling have been described to affect cardiac morphogenesis [8,9] and several members of the wnt-frizzled signal transduction pathway were found to be expressed during cardiac development in vertebrates [10–14].

In cardiovascular pathology, re-expression of a fetal gene expression pattern is a generally observed phenomenon [15]. The . . . [Full Text of this Article]


    2. Brief outline of the wnt-frizzled cascade
 

    3. The wnt-frizzled pathway and cardiac wound healing after myocardial infarction
 

    4. The wnt-frizzled cascade and angiogenesis/neovascularization
 

    5. The wnt-frizzled cascade, cardiac hypertrophy and heart failure
 

    6. The wnt-frizzled cascade and arterial injury
 

    7. Conclusions
 

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