Journal
CARDIOVASCULAR DRUGS AND THERAPY
Volume 28, Issue 3, Pages 237-246Publisher
SPRINGER
DOI: 10.1007/s10557-014-6520-2
Keywords
Galectin-3; Biomarker; Heart failure; Cardiac remodeling; Fibrosis
Funding
- Abbott
- BG Medicine
- Netherlands Organisation for Scientific Research, NWO VIDI grant [917.13.350]
- AstraZeneca
- Biomerieux
- Pfizer
- Baxter
- Novartis
- Swiss National Science Foundation
- Swiss Heart Foundation
- Cardiovascular Research Foundation Basel
- Alere
- Brahms
- Critical Diagnostics
- Nanosphere
- Roche
- Siemens
- University Basel
- University Hospital Basel
- Bristol-Myers Squibb
- BRAHMS GmbH
- EU FP7 Programme
- Vifor Int.
- Medicines Company
- Cardiorentis
- Daiichi-Sankyo
- GE
- Janssen
- Lilly
- Singulex
- Verathon
- Roche Diagnostics
- EFG Diagnostics
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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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