Myocardial galectin-3 is upregulated upon cardiac stressors such as angiotensin II and pressure overload leading to cardiac remodeling and heart failure. The expression level of galectin-3 mirrors the progression and severity of heart failure and therefore, galectin-3 is being used as a biomarker for heart failure. However, as galectin-3 is causally involved in pathological myocardial fibrosis it has been suggested that galectin-3 also actively contributes to heart failure development. In this review we discuss how galectin-3 could be a target for therapy in heart failure. Currently, attempts are being made to target or inhibit galectin-3 using natural or pharmaceutical inhibitors with the aim to ameliorate heart failure. Available experimental evidence suggests that galectin-3 inhibition indeed may represent a novel tool to treat heart failure. A strong interaction with aldosterone, another strong pro-fibrotic factor, has been described. Clinical studies are needed to prove if galectin-3 may be used to install specific treatment regimens.
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Atrial natriuretic peptide
Coronary artery disease
Carbohydrate recognition domain
Cardiac resynchronization therapy
Heart failure with preserved ejection fraction
Implantable cardioverter defibrillator
Left ventricular end diastolic pressure
Modified citrus pectin
Mineralocorticoid receptor antagonist
N-terminal pro B-type natriuretic peptide
Sympathetic nervous system
Transverse aortic constriction
Vascular smooth muscle cell
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Conflict of Interest
Rudolf A. de Boer has received research grants from Abbott, BG Medicine, and Netherlands Organisation for Scientific Research, NWO VIDI grant (No. 917.13.350); consultancy and/or speaker fees from Abbott, AstraZeneca, Biomérieux, BG Medicine, Pfizer, Baxter, and Novartis; and ownership interest in Pectacea. Christian Mueller has received research grants from Swiss National Science Foundation, the Swiss Heart Foundation, the Cardiovascular Research Foundation Basel, Abbott, Alere, Brahms, Critical Diagnostics, Nanosphere, Roche, Siemens, the University Basel, and the University Hospital Basel; and consultancy and/or speaker fees from Abbott, Alere, Brahms, BG Medicine, Novartis, AstraZeneca, Bristol-Myers Squibb, Roche, and Siemens. Dirk J. van Veldhuisen has received research grants from BG Medicine and consultancy and/or speaker fees from BG Medicine. Stefan D. Anker has received research grants from BRAHMS GmbH, EU FP7 Programme, and consultancy and/or speaker fees from BG Medicine, BRAHMS GmbH, and Vifor Int. W. Frank Peacock has received research grants from Abbott, Alere, Brahms, Novartis, Roche, and The Medicines Company; consultancy and/or speaker fees from Abbott, Alere, AstraZeneca, BG Medicine, Cardiorentis, Daiichi-Sankyo, GE, Janssen, Lilly, The Medicines Company, Singulex, and Verathon; and ownership interest in Comprehensive Research Associates LLC, Vital Sensors, and Emergencies in Medicine LLC. Kirkwood F. Adams has received research grants from Roche Diagnostics and Critical Diagnostics, and consultancy and/or speaker fees from BG Medicine, Roche Diagnostics, and Critical Diagnostics. Alan Maisel has received research grants from Alere, Abbott, BG Medical, and Brahms; consultancy and/or speaker fees from Alere, Critical Diagnostics, Sphingotec, BG Medicine, and EFG Diagnostics; and is co-founder of Cardero Therapeutics and MyLife Diagnostics. The authors have no other funding, financial relationships, or conflicts of interest to disclose.
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de Boer, R.A., van der Velde, A.R., Mueller, C. et al. Galectin-3: A Modifiable Risk Factor in Heart Failure. Cardiovasc Drugs Ther 28, 237–246 (2014). https://doi.org/10.1007/s10557-014-6520-2
- Heart failure
- Cardiac remodeling