Galectin-3: A Modifiable Risk Factor in Heart Failurede Boer, R. A., van der Velde, A. R., Mueller, C., van Veldhuisen, D. J., Anker, S. D., Peacock, W. F., Adams, K. F. & Maisel, A., Jun-2014, In : Cardiovascular Drugs and Therapy. 28, 3, p. 237-246 10 p.
Research output: Contribution to journal › Review article › Academic › peer-review
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.
|Number of pages||10|
|Journal||Cardiovascular Drugs and Therapy|
|Publication status||Published - Jun-2014|
- Galectin-3, Biomarker, Heart failure, Cardiac remodeling, Fibrosis, PRESERVED EJECTION FRACTION, MODIFIED CITRUS PECTIN, PROGNOSTIC VALUE, HF-ACTION, FIBROSIS, INHIBITION, MARKER, MORTALITY, CANCER, MACROPHAGES