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European Journal of Heart Failure Advance Access originally published online on July 31, 2009
European Journal of Heart Failure 2009 11(9):811-817; doi:10.1093/eurjhf/hfp097
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Galectin-3: a novel mediator of heart failure development and progression

Rudolf A. de Boer1,*, Adriaan A. Voors1, Pieter Muntendam2, Wiek H. van Gilst1 and Dirk J. van Veldhuisen1

1 Department of Cardiology, University Medical Centre Groningen, PO Box 30.001, Hanzeplein 1, 9700 RB, Groningen, The Netherlands
2 BG Medicine, Inc., Waltham, MA, USA

* Corresponding author. Tel: +31 50 361 2355, Fax: +31 50 361 1347, Email: r.a.de.boer{at}thorax.umcg.nl


  Abstract

Galectins are a family of soluble β-galactoside-binding lectins that play many important regulatory roles in inflammation, immunity, and cancer. Recently, a role for galectin-3 in the pathophysiology of heart failure (HF) has been suggested. Numerous studies have demonstrated the up-regulation of galectin-3 in hypertrophied hearts, its stimulatory effect on macrophage migration, fibroblast proliferation, and the development of fibrosis. The latter observation is particularly relevant as cardiac remodelling is an important determinant of the clinical outcome of HF and is linked to disease progression and poor prognosis. Because galectin-3 expression is maximal at peak fibrosis and virtually absent after recovery, routine measurement in patients with HF may prove valuable to identify those patients at highest risk for readmission or death, thus enabling physicians to tailor the level of care to individual patient needs. This review summarizes the most recent advances in galectin-3 research, with an emphasis on the role galectin-3 plays in the development and progression of HF.

Key Words: Galectin 3 • Heart failure • Prognosis • Fibrosis • Macrophages • Biomarkers

Received February 12, 2009; Revised May 28, 2009; Accepted June 10, 2009


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